subject:(Macrophages)

Penn State University

1. Carroll, Melissa Anne. STAT3-Deficiency in Bone Marrow Hematopoietic Stem Cells results in Dysfunctional Macrophages and Correlates with Crohn's Disease-like Pathogenesis .

Degree: 2011, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/11611

► The most well-known subsets of inflammatory bowel disease (IBD) are ulcerative colitis (UC) and Crohn’s Disease (CD). Currently, the etiology of CD is unknown but… (more)

▼ The most well-known subsets of inflammatory bowel disease (IBD) are ulcerative colitis (UC) and Crohn’s Disease (CD). Currently, the etiology of CD is unknown but it is thought to result from excessive T helper (Th)1-cell mediated inflammation. There is no gender or age bias, but CD is most often detected between 15-30 years of age. Macrophages are tissue specific monocytes and are the first line of defense in innate immunity; once activated they produce interleukin (IL)-12, IL23 and tumor necrosis factor-alpha (TNFá), proinflammatory cytokines, which induce a Th1-cell mediated immune response. Th1-cells can synthesize several proinflammatory cytokines including IL6, TNFá and interferon-gamma (IFNã). Signal transducers and activators of transcription (STAT) proteins play an important role in mediating intestinal cytokine signaling and it is unknown if the loss of these proteins initiate severe downstream modifications that consequently result in CD. When compensating for a deficiency in STAT3, STAT1 levels increase, which leads to an increase in IFNã signaling, which promotes Th1-cell mediated inflammation. IL10, which is mediated through STAT3 signaling, is an anti-inflammatory cytokine that is secreted from activated macrophages. IL10 inhibits excessive macrophage activation which suppresses the macrophage induced synthesis of TNFá, and thus is responsible for down-regulating Th1-cell mediated immune responses. This suggests that STAT3 mediates mucosal immune tolerance during an innate immune response. Breeding a bone marrow (B)-TIE2 promoter driven Cre recombinase gene- targeted mouse with a STAT3 lox-P (F/F) mouse created a conditional (specific to bone marrow hematopoietic stem cells) STAT3 knock-out. This tissue specific STAT3 deficient mouse is suitable for in vivo studies because it exhibits a spontaneous Crohn’s-like pathogenesis in the small and large intestines, also characterized by an over production of pro-inflammatory cytokines and excessive macrophage infiltrations. In addition to these morphological changes, one functional change demonstrated a loss of NADPH oxidase activity, which is an important response induced by the innate immune system to kill phagocytosed materials (Welte et al., 2003). The overall goal of this project was to determine the role of STAT1 and STAT3 signaling in the development of inflammatory bowel disease. My working hypothesis was that defective innate immunity in Crohn’s disease may correlate with a loss in STAT3 activity. My specific hypothesis was that STAT3-deficiency in bone marrow hematopoietic stem cells results in dysfunctional macrophages and correlates with Crohn’s Disease-like pathogenesis. In conclusion, this study determined that STAT3 signaling is required for normal macrophage functions and that abnormal macrophages critical for the pathogenesis of a Crohn’s-like disease in these mice models. It was demonstrated that the role of STAT3 activity in monocyte development and function has a regulatory function, for differentiating numbers and… Advisors/Committee Members: Samuel Shaomin Zhang, Dissertation Advisor/Co-Advisor, Samuel Shaomin Zhang, Committee Chair/Co-Chair, Colin James Barnstable, Committee Member, Patricia Mc Laughlin, Committee Member, Lisa S Poritz, Committee Member.

Subjects/Keywords: macrophages

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APA (6^th Edition):

Carroll, M. A. (2011). STAT3-Deficiency in Bone Marrow Hematopoietic Stem Cells results in Dysfunctional Macrophages and Correlates with Crohn's Disease-like Pathogenesis . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/11611

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Carroll, Melissa Anne. “STAT3-Deficiency in Bone Marrow Hematopoietic Stem Cells results in Dysfunctional Macrophages and Correlates with Crohn's Disease-like Pathogenesis .” 2011. Thesis, Penn State University. Accessed March 02, 2021. https://submit-etda.libraries.psu.edu/catalog/11611.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Carroll, Melissa Anne. “STAT3-Deficiency in Bone Marrow Hematopoietic Stem Cells results in Dysfunctional Macrophages and Correlates with Crohn's Disease-like Pathogenesis .” 2011. Web. 02 Mar 2021.

Vancouver:

Carroll MA. STAT3-Deficiency in Bone Marrow Hematopoietic Stem Cells results in Dysfunctional Macrophages and Correlates with Crohn's Disease-like Pathogenesis . [Internet] [Thesis]. Penn State University; 2011. [cited 2021 Mar 02]. Available from: https://submit-etda.libraries.psu.edu/catalog/11611.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Carroll MA. STAT3-Deficiency in Bone Marrow Hematopoietic Stem Cells results in Dysfunctional Macrophages and Correlates with Crohn's Disease-like Pathogenesis . [Thesis]. Penn State University; 2011. Available from: https://submit-etda.libraries.psu.edu/catalog/11611

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Aberdeen

2. Kluge, Christina, E. Regulating human Th17 polarisation by activated macrophages.

Degree: School of Medicine and Dentistry., 2012, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=185639 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=185639&custom_att_2=simple_viewer

Subjects/Keywords: Macrophages

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APA (6^th Edition):

Kluge, Christina, E. (2012). Regulating human Th17 polarisation by activated macrophages. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=185639 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=185639&custom_att_2=simple_viewer

Chicago Manual of Style (16^th Edition):

Kluge, Christina, E. “Regulating human Th17 polarisation by activated macrophages.” 2012. Doctoral Dissertation, University of Aberdeen. Accessed March 02, 2021. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=185639 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=185639&custom_att_2=simple_viewer.

MLA Handbook (7^th Edition):

Kluge, Christina, E. “Regulating human Th17 polarisation by activated macrophages.” 2012. Web. 02 Mar 2021.

Vancouver:

Kluge, Christina E. Regulating human Th17 polarisation by activated macrophages. [Internet] [Doctoral dissertation]. University of Aberdeen; 2012. [cited 2021 Mar 02]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=185639 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=185639&custom_att_2=simple_viewer.

Council of Science Editors:

Kluge, Christina E. Regulating human Th17 polarisation by activated macrophages. [Doctoral Dissertation]. University of Aberdeen; 2012. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=185639 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=185639&custom_att_2=simple_viewer

University of Arizona

3. Elvick, Allen LeRoy, 1942-. Enzyme profiles of control and sulfuric acid aerosol stressed alveolar macrophages .

Degree: 1978, University of Arizona

URL: http://hdl.handle.net/10150/348276

Subjects/Keywords: Macrophages.

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APA (6^th Edition):

Elvick, Allen LeRoy, 1. (1978). Enzyme profiles of control and sulfuric acid aerosol stressed alveolar macrophages . (Masters Thesis). University of Arizona. Retrieved from http://hdl.handle.net/10150/348276

Chicago Manual of Style (16^th Edition):

Elvick, Allen LeRoy, 1942-. “Enzyme profiles of control and sulfuric acid aerosol stressed alveolar macrophages .” 1978. Masters Thesis, University of Arizona. Accessed March 02, 2021. http://hdl.handle.net/10150/348276.

MLA Handbook (7^th Edition):

Elvick, Allen LeRoy, 1942-. “Enzyme profiles of control and sulfuric acid aerosol stressed alveolar macrophages .” 1978. Web. 02 Mar 2021.

Vancouver:

Elvick, Allen LeRoy 1. Enzyme profiles of control and sulfuric acid aerosol stressed alveolar macrophages . [Internet] [Masters thesis]. University of Arizona; 1978. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/10150/348276.

Council of Science Editors:

Elvick, Allen LeRoy 1. Enzyme profiles of control and sulfuric acid aerosol stressed alveolar macrophages . [Masters Thesis]. University of Arizona; 1978. Available from: http://hdl.handle.net/10150/348276

University of Hong Kong

4. 彭佼. Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin.

Degree: 2015, University of Hong Kong

URL: http://hdl.handle.net/10722/216268

► Tumor-associated macrophages (TAMs) play a key role in the escape of tumor cells from immune surveillance. “Re-programming” TAMs to switch from a M2 to a… (more)

▼ Tumor-associated macrophages (TAMs) play a key role in the escape of tumor cells from immune surveillance. “Re-programming” TAMs to switch from a M2 to a M1-type phenotype and thereby restore tumor specific immune responses that are protective continues stimulate considerable scientific interest in the field of tumor biology. The aims of this study focus on: 1) to identify the inhibition of TGF-β signaling in combination with TLR7 ligation could re-program the phenotype of TAMs and increase their tumoricidal activities; 2) to investigate that adiponectin (APN) deficiency can promote TAMs polarization towards a M1-like phenotype and reduce tumor progression in murine sarcoma model. TGF-β plays a multi-functional role in tumor development including modulating the biological activity of both the tumor and TAMs. In a TAM/tumor cell co-culture system in which both cells were isolated from murine sarcoma model, I found inhibition of TGF-β signaling with TGF-β receptor I inhibitor in combination with TLR7 ligation could re-program TAMs to the M1-like type, evidenced by: 1) up-regulating the expression of M1-like type marker iNOS, CD80 and MHCII in TAMs; 2) down-regulating the expression of VEGF and CD31 to suppress angiogenesis; 3) increasing tumoricidal activity of TAMs and inducing tumor cells apoptosis and 4) elevating infiltration of inflammatory immune cells 〖CD4〗^+,〖 CD8〗^+ T cells and neutrophils in tumor mass. Mechanistically, it was also found that combination treatment could enhance NF-кB activation through up-regulating TRAF6 expression and increasing NF-кB nuclear translocation. APN, anti-inflammatory adipokine, has been shown to promote macrophage polarization to a M2 type in vitro. In the present study, APN and TAMs have high expression in infantile rhabdomyosarcoma, particularly in its malignant subtype. The study was then extended to investigate the effect of APN on TAMs polarization by murine MN/MCA1 sarcoma model. The results showed that exogenous APN had no direct effect on MN/MCA1 proliferation but tumor size was sharply reduced in 〖apn〗^(-/-) mice compared to their wild type counterparts. Next, my study demonstrates that the accumulation of TAMs in 〖apn〗^(-/-) mice was reduced correlated to down-regulation of serum MCP-1. Furthermore, TAMs showed a M1-like phenotype with a marked increase in the 〖MHCII 〗^highpopulation. Quantitative PCR analysis indicated that iNOS was increased, whereas the M2 markers IL-10 and YM1 were decreased. Increased TNF-α and reduced IL-10 were also observed in the serum and TAMs of 〖apn〗^(-/-) mice. In addition, APN deficiency increased frequency of CD4+, CD8+ T cells and NK cells in the tumors and down-regulated MMP-9 and collagen to suppress tumor metastasis. Moreover, p-p38 was sharply decreased in TAMs of 〖apn〗^(-/-) mice and adoption of p38 MAPK inhibitor could significantly reduce tumor size and increase MHCII expression in wild type mice, which suggested that APN regulated p38 MAPK signaling pathway may involve in TAMs polarization. In summary, the present study…

Subjects/Keywords: Macrophages

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

彭佼. (2015). Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/216268

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

彭佼. “Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin.” 2015. Thesis, University of Hong Kong. Accessed March 02, 2021. http://hdl.handle.net/10722/216268.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

彭佼. “Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin.” 2015. Web. 02 Mar 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

彭佼. Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin. [Internet] [Thesis]. University of Hong Kong; 2015. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/10722/216268.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

彭佼. Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin. [Thesis]. University of Hong Kong; 2015. Available from: http://hdl.handle.net/10722/216268

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Duquesne University

5. Rogers, Walter John. Factors Effecting Uptake and Visualization of Superparamagnetic Iron Oxide Particles by Macrophages: Relevance for Use in MRI Plaque Imaging.

Degree: PhD, Chemistry and Biochemistry, 2003, Duquesne University

URL: https://dsc.duq.edu/etd/1117

► Cardiovascular disease kills nearly 1 million Americans each year. While treatment at all levels has made significant advances over the past 3 decades, diagnosis is… (more)

▼ Cardiovascular disease kills nearly 1 million Americans each year. While treatment at all levels has made significant advances over the past 3 decades, diagnosis is still limited to structural or hemodynamic changes associated with advanced disease. More than 60% of myocardial infarctions (MI) result from the rupture and associated acute thrombosis of atherosclerotic plaque that reduce lumen size by less that 50%. Ultra small superparamagnetic iron oxide particles (USPIO) have recently been proposed as a macrophage targeted magnetic resonance contrast agent. The goal of the present study was to determine if, and the extent to which, molecules known to alter macrophage metabolism significantly alter the extent to which USPIO's are internalized in these cells. Murine macrophage cells (J774) known to be constitutively activated, were cultured in 8 well chamber slides. One group of 4 wells was treated for 24 hours with the test agent. Control and treated cells were then incubated for 4 hours with 0.0µL, 1.0 µL (11.2 µg Fe), 10.0 µL (112.0 µg Fe) and 100.0 µL (1.12 mg Fe) of stock USPIO (Feridex, Berlex labs). Cell density and iron uptake was quantified using spectral analysis of digital microscope images of fixed cells stained with acridine orange and counterstained with Prussian Blue. Macrophage uptake of USPIO was significantly related to iron concentration (r2= 0.992). However there was saturation of cell uptake at higher USPIO concentration. Uptake, (iron area/total image area) expressed as the percent, became significantly greater than background by 5 minutes (0.084+ 0.001% versus 0.045 +0.029%, p=0.028) and peaked at 4 hours. At low dose (10 and 20 ng/ml) Interleukin-4 did not affect cell uptake of USPIO. However at 40 ng/ml, IL-4 produced a significant increase in iron endocytosis at 1.12 mg Fe/ml (2-way ANOVA, p=0.032). Similarly, Human Interferon gamma (IFN-γ) had no effect at the 3 lower doses (10, 100, and 500 International Units (IU)/ml, corresponding to 0.5, 5.0, 25.0 and 50 ng/ml). Treatment with 1000 IU/ml resulted in an increase in cell uptake (2-way ANOVA, p=0.045). To test the importance of serum proteins on endocytosis, a group of cells were cultured with and without 10% fetal bovine serum (FBS). Absence of FBS resulted in a substantial reduction in USPIO uptake (p < 0.001). There was also a trend toward reduced cell density compared to control (p=0.056) which is likely the effect of the absence of growth factors in the FBS free cell cultures. Cytochalsin-B depolarizes actin filaments within macrophage plasma membrane and thus inhibits membrane invagination and thus endocytosis. At a dose of 1.0 µg/ml it has been previously been shown to preferentially inhibit endocytosis of larger particles (> 300 nm) with little effect on small (< 300 nm). In the present study, USPIO uptake trended toward being reduced (p=0.062) indicating that although individual particle size was small (100-150 nm), the aggregation of these particles… Advisors/Committee Members: Partha Basu, John A. Pollack, Mitchell E. Johnson, Robert W. W. Biederman.

Subjects/Keywords: macrophages

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APA (6^th Edition):

Rogers, W. J. (2003). Factors Effecting Uptake and Visualization of Superparamagnetic Iron Oxide Particles by Macrophages: Relevance for Use in MRI Plaque Imaging. (Doctoral Dissertation). Duquesne University. Retrieved from https://dsc.duq.edu/etd/1117

Chicago Manual of Style (16^th Edition):

Rogers, Walter John. “Factors Effecting Uptake and Visualization of Superparamagnetic Iron Oxide Particles by Macrophages: Relevance for Use in MRI Plaque Imaging.” 2003. Doctoral Dissertation, Duquesne University. Accessed March 02, 2021. https://dsc.duq.edu/etd/1117.

MLA Handbook (7^th Edition):

Rogers, Walter John. “Factors Effecting Uptake and Visualization of Superparamagnetic Iron Oxide Particles by Macrophages: Relevance for Use in MRI Plaque Imaging.” 2003. Web. 02 Mar 2021.

Vancouver:

Rogers WJ. Factors Effecting Uptake and Visualization of Superparamagnetic Iron Oxide Particles by Macrophages: Relevance for Use in MRI Plaque Imaging. [Internet] [Doctoral dissertation]. Duquesne University; 2003. [cited 2021 Mar 02]. Available from: https://dsc.duq.edu/etd/1117.

Council of Science Editors:

Rogers WJ. Factors Effecting Uptake and Visualization of Superparamagnetic Iron Oxide Particles by Macrophages: Relevance for Use in MRI Plaque Imaging. [Doctoral Dissertation]. Duquesne University; 2003. Available from: https://dsc.duq.edu/etd/1117

University of Aberdeen

6. Kluge, Christina. Regulating human Th17 polarisation by activated macrophages.

Degree: PhD, 2012, University of Aberdeen

URL: https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12153080130005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.553806

► Inflammatory diseases such as autoimmune and atopic diseases are a common problem worldwide. Although there have been substantial advances in medical therapies, current treatments are… (more)

▼ Inflammatory diseases such as autoimmune and atopic diseases are a common problem worldwide. Although there have been substantial advances in medical therapies, current treatments are not able to cure these conditions. In order to develop more specific, individually targeted and efficient treatments, a better understanding of the cells, mediators and mechanisms that lead to pathology are necessary. Macrophages and T cells are major players in the human immune system. Despite the abundance of macrophages at inflammatory sites and their secretion of T cell polarising cytokines, their roles as antigen presenting cells has been overlooked until now. This PhD project aimed to determine, firstly, the contribution of differentially activated human macrophages in the regulation of adaptive immune responses in inflammation with the main focus on the pro‐inflammatory T cell subset Th17, secondly, how macrophage functions could be modified to alter T cell polarisation and thirdly, how novel alternative mechanisms using electric fields can alter T cell responses. I demonstrate for the first time that macrophages can efficiently induce T cell polarisation and Th17 differentiation in response to recall and primary antigens and that the specific macrophage activation state is essential to drive Th17 responses. This suggests that macrophages are an important stimulus contributing to pathogenic T cell responses in human inflammatory diseases. Importantly, both memory and naïve T cells gave rise to Th17 cells following culture with antigen‐loaded activated macrophages, where non‐specific effects of mitogenic activation were avoided. Targeting human macrophage signalling pathways through SOCS3, reduced their pro‐inflammatory potential and Th17 polarising ability, pointing to SOCS3 as an effective therapeutic target. As an alternative approach, I demonstrate here that small electric fields of physiological strength strongly influence immune responses and significantly dampen Th17 differentiation. This suggests that EFs have the potential to facilitate healing processes or support conventional therapies for inflammatory diseases. Overall, these data present a strong basis for the development novel treatment possibilities for inflammatory diseases that are distinct from the currently used conventional therapies.

Subjects/Keywords: 616.07995; Macrophages

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APA (6^th Edition):

Kluge, C. (2012). Regulating human Th17 polarisation by activated macrophages. (Doctoral Dissertation). University of Aberdeen. Retrieved from https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12153080130005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.553806

Chicago Manual of Style (16^th Edition):

Kluge, Christina. “Regulating human Th17 polarisation by activated macrophages.” 2012. Doctoral Dissertation, University of Aberdeen. Accessed March 02, 2021. https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12153080130005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.553806.

MLA Handbook (7^th Edition):

Kluge, Christina. “Regulating human Th17 polarisation by activated macrophages.” 2012. Web. 02 Mar 2021.

Vancouver:

Kluge C. Regulating human Th17 polarisation by activated macrophages. [Internet] [Doctoral dissertation]. University of Aberdeen; 2012. [cited 2021 Mar 02]. Available from: https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12153080130005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.553806.

Council of Science Editors:

Kluge C. Regulating human Th17 polarisation by activated macrophages. [Doctoral Dissertation]. University of Aberdeen; 2012. Available from: https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12153080130005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.553806

7. Naiken, Tanesha. Étude de la reprogrammation métabolique dans les macrophages polarisés : Exploring cell metabolism reprogramming in polarized macrophages.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2014, Nice

URL: http://www.theses.fr/2014NICE4039

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Les cellules tumorales requièrent un approvisionnement continu de nutriments pour produire de l’énergie. Cependant le micro-environnement autour de la tumeur en fournit une quantité insuffisante.… (more)

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Les cellules tumorales requièrent un approvisionnement continu de nutriments pour produire de l’énergie. Cependant le micro-environnement autour de la tumeur en fournit une quantité insuffisante. Nous avons donc émis l'hypothèse qu'il existe une symbiose nutritionnelle entre les cellules stromales et les cellules tumorales, qui contribue à la tumorigenèse et, nous nous sommes concentrés sur les macrophages. Typiquement, ils sont classés comme classiques (M1-like) ou alternatifs (M2-like) et dans le stroma, les macrophages ont tendance à avoir un phénotype M2-like. Concernant leur profil métabolique, les macrophages M1-like ont un métabolisme glycolytique. Toutefois, les caractéristiques métaboliques des macrophages M2-like ne sont toujours pas clairement définies. Dans nos travaux, en utilisant la lignée cellulaire murine de macrophage, les RAW 264.7, nous avons confirmé que les macrophages M1-like sont exclusivement glycolytiques alors que les M2-like ont plutôt un profil oxydatif. Nous avons démontré qu’il existe une certaine plasticité métabolique des cellules M2-likes car elles sont capables de basculer vers la glycolyse quand la respiration mitochondriale est inhibée. De plus, un blocage de la glycolyse n'a révélé aucune adaptation métabolique des macrophages M1-like mais influe sur les cellules M2, en réduisant leur capacité respiratoire. Finalement, nous avons observé que la polarisation fonctionnelle des macrophages M1-like pourrait être affectée par des changements dans le métabolisme cellulaire. Ces données suggèrent que le métabolisme est un facteur déterminant du phénotype fonctionnel des macrophages.

Tumor cells require a constant supply of nutrients and yet, their tumor microenvironment supplies insufficient amount of nutrients. We therefore hypothesize that it exists a nutritional symbiosis between stromal cells and tumor cells which contribute to tumorigenesis. Of these stromal cells, we focused on macrophages. Typically, they are classified as inflammatory (M1-like) or alternative (M2-like) and within the stroma, macrophages tend to exhibit an M2-like phenotype. Concerning their metabolic profile, M1-like macrophages have been described to exhibit a glycolytic metabolism. However, the metabolic features of M2-like macrophages remain pretty unclear. In our work, using the mouse monocyte macrophage cell line RAW 264.7, we have confirmed that M1-like cells are exclusively glycolytic whereas M2-like macrophages appear as mainly oxidative. We were able to demonstrate some metabolic plasticity for M2 cells that shift to glycolysis when mitochondrial respiration is inhibited. The targeting of glycolysis through the blockade of downstream lactic acid export catalyzed by monocarboxylate transporters, did not reveal any metabolic adaptation of M1-like macrophages but impacted on M2 cells, reducing their respiratory rate. By manipulating metabolic features of M1- and M2-like macrophages (i.e. glycolysis vs oxidative phosphorylation), we also investigated whether metabolic pathways themselves could impact on…

Advisors/Committee Members: Pouysségur, Jacques (thesis director).

Subjects/Keywords: Métabolisme; Cancer; Macrophages; Metabolism; Cancer; Macrophages

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APA (6^th Edition):

Naiken, T. (2014). Étude de la reprogrammation métabolique dans les macrophages polarisés : Exploring cell metabolism reprogramming in polarized macrophages. (Doctoral Dissertation). Nice. Retrieved from http://www.theses.fr/2014NICE4039

Chicago Manual of Style (16^th Edition):

Naiken, Tanesha. “Étude de la reprogrammation métabolique dans les macrophages polarisés : Exploring cell metabolism reprogramming in polarized macrophages.” 2014. Doctoral Dissertation, Nice. Accessed March 02, 2021. http://www.theses.fr/2014NICE4039.

MLA Handbook (7^th Edition):

Naiken, Tanesha. “Étude de la reprogrammation métabolique dans les macrophages polarisés : Exploring cell metabolism reprogramming in polarized macrophages.” 2014. Web. 02 Mar 2021.

Vancouver:

Naiken T. Étude de la reprogrammation métabolique dans les macrophages polarisés : Exploring cell metabolism reprogramming in polarized macrophages. [Internet] [Doctoral dissertation]. Nice; 2014. [cited 2021 Mar 02]. Available from: http://www.theses.fr/2014NICE4039.

Council of Science Editors:

Naiken T. Étude de la reprogrammation métabolique dans les macrophages polarisés : Exploring cell metabolism reprogramming in polarized macrophages. [Doctoral Dissertation]. Nice; 2014. Available from: http://www.theses.fr/2014NICE4039

8. Mossadegh Rashti, Noushin. Ontogeny of testicular macrophages, the guardians of fertility : Ontogénie des macrophages testiculaires, les gardiens de la fertilité.

Degree: Docteur es, Immunologie, 2018, Aix Marseille Université

URL: http://www.theses.fr/2018AIXM0141

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Les macrophages sont des cellules de l’immunité innée et sont localisés dans la majorité des organes du corps, présentant des fonctions spécifiques dépendant de leur… (more)

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Les macrophages sont des cellules de l’immunité innée et sont localisés dans la majorité des organes du corps, présentant des fonctions spécifiques dépendant de leur lieu de résidence.Les macrophages d’origine embryonnaire sont la source majeure des macrophages tissulaires et sont capables de se maintenir à long terme dans la plupart des organes adultes.Cependant, il reste certains organes comme le testicule, où l’origine des macrophages n’est pas clairement déterminée. Le testicule est considéré comme un organe immuno-privilégié et a cette nécessité de protéger de tous contacts les spermatozoïdes des cellules immunitaires, qui pourraient induire une auto-immunité.Les macrophages testiculaires (tMφ) contribuent à maintenir ce statut d’organe immuno-privilégié en produisant des cytokines immunosuppressives. Pour ces raisons, les tMφ peuvent être considérés comme des “ gardiens de la fertilité”. Dans les testicules adultes, deux différentes populations de macrophages, nommées interstitielles et péritubulaires, ont été identifiées en se basant sur leurs morphologies et localisations distinctes, mais leur origine et leur mode de développement et de maintenance restent encore inconnus. En combinant des méthodes de traçage cellulaire et la mise au point d’un modèle de transfert adoptif dans des souriceaux, j’ai démontré que les macrophages d’origine embryonnaire contribuaient exclusivement à la population de tMφ interstitielle dès la naissance et que les tMφ péritubulaires proviennent exclusivement de la moelle osseuse. Après avoir caractérisé les tMφ, mes prochaines investigations se porteront sur l’étude des fonctions de chacune de ces deux populations.

Macrophages are innate immune cells residing in most of the organs of the body and ensure proper organ function. Traditionally, it has been known that macrophages can be derived from HSC progenitors in the bone-marrow (BM), but technology using fate-mapping tools has revealed that macrophages can already be generated from embryonic progenitors. Embryo-derived macrophages are a major source of tissue-resident macrophages and can self-maintain during adulthood. The origin of resident macrophages in the testis, however, so far has not been well studied.Importantly, the testis is considered as an immune-privileged organ by protecting the highly immunogenic spermatozoa sequestrated in the seminiferous tubules from the entrance of immune cells. In the adult testis, macrophages participate in the creation of an immune suppressive microenvironment preventing auto-immune attack. Therefore, testicular macrophages tMφ could be considered as the guardians of fertility. Recently,two different macrophage populations have been identified in the adult testis, called interstitial and peritubular, based on their distinct localization and morphology,but their developmental origin and homeostatic maintenance were unknown.Combining the genetic lineage tracing and the neonatal adoptive transfer model, I could demonstrate that the embryo-derived macrophages give rise exclusively to…

Advisors/Committee Members: Sieweke, Michael H. (thesis director).

Subjects/Keywords: Macrophages; Ontogenie; Testicule; Macrophages; Ontogeny; Testis; 571

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APA (6^th Edition):

Mossadegh Rashti, N. (2018). Ontogeny of testicular macrophages, the guardians of fertility : Ontogénie des macrophages testiculaires, les gardiens de la fertilité. (Doctoral Dissertation). Aix Marseille Université. Retrieved from http://www.theses.fr/2018AIXM0141

Chicago Manual of Style (16^th Edition):

Mossadegh Rashti, Noushin. “Ontogeny of testicular macrophages, the guardians of fertility : Ontogénie des macrophages testiculaires, les gardiens de la fertilité.” 2018. Doctoral Dissertation, Aix Marseille Université. Accessed March 02, 2021. http://www.theses.fr/2018AIXM0141.

MLA Handbook (7^th Edition):

Mossadegh Rashti, Noushin. “Ontogeny of testicular macrophages, the guardians of fertility : Ontogénie des macrophages testiculaires, les gardiens de la fertilité.” 2018. Web. 02 Mar 2021.

Vancouver:

Mossadegh Rashti N. Ontogeny of testicular macrophages, the guardians of fertility : Ontogénie des macrophages testiculaires, les gardiens de la fertilité. [Internet] [Doctoral dissertation]. Aix Marseille Université 2018. [cited 2021 Mar 02]. Available from: http://www.theses.fr/2018AIXM0141.

Council of Science Editors:

Mossadegh Rashti N. Ontogeny of testicular macrophages, the guardians of fertility : Ontogénie des macrophages testiculaires, les gardiens de la fertilité. [Doctoral Dissertation]. Aix Marseille Université 2018. Available from: http://www.theses.fr/2018AIXM0141

9. Benkdane, Merieme. Rôle protecteur des cellules de Küpffer de phénotype M2 anti-inflammatoire dans la maladie alcoolique du foie : Protective role of M2 anti-inflammatory Kupffer cells in alcoholic liver disease.

Degree: Docteur es, Physiopathologie, 2012, Université Paris-Est

URL: http://www.theses.fr/2012PEST0062

► L'alcool est la première cause de maladie hépatique en France, et la maladie alcoolique du foie est responsable de près de 7000 décès par an.… (more)

▼ L'alcool est la première cause de maladie hépatique en France, et la maladie alcoolique du foie est responsable de près de 7000 décès par an. La surcharge graisseuse est la troisième cause de maladie hépatique, et s'inscrit dans le cadre plus large du syndrome métabolique. La physiopathologie de ces deux types de maladies hépatiques est très similaire. La stéatose, définie par l'accumulation excessive de triglycérides dans le foie, est la première lésion retrouvée chez les patients. La stéatose peut évoluer vers la stéato‐hépatite lorsqu'elle est associée à une inflammation, une mort hépatocytaire, et à l'initiation d'une réponse fibrogénique. La stéato‐hépatite évolue parfois vers la cirrhose, stade ultime avant le carcinome hépatocellulaire. Il n'existe à ce jour aucun traitement efficace de ces maladies hormis le sevrage alcoolique dans le cadre de la maladie alcoolique du foie et un régime associé à de l'exercice dans le cadre de la maladie hépatique d'origine non‐alcoolique. Il est donc urgent d'identifier de nouvelles stratégies thérapeutiques pour lutter contre la progression de ces maladies.L'activation des cellules de Küpffer, les macrophages résidents du foie, joue un rôle déterminant dans le processus inflammatoire qui initie l'atteinte hépatique. Comme tous les macrophages, les cellules de Küpffer peuvent adopter tout un spectre de phénotypes parmi lesquels on distingue deux extrêmes : le phénotype M1 ou pro‐inflammatoire et le phénotype M2 ou anti‐inflammatoire. Les données de la littérature ainsi que celles préalablement obtenues par le laboratoire d'accueil ont établi les effets délétères d'une polarisation pro‐inflammatoire M1 des cellules de Küpffer sur l'évolution de la maladie hépatique d'origine alcoolique ou non alcoolique. Cependant, aucune étude n'avait examiné l'impact d'une polarisation anti‐inflammatoire (M2) des cellules de Küpffer sur ces maladies.L'objectif de ce travail a été d'évaluer si favoriser la polarisation des cellules de Küpffer vers un phénotype M2 anti‐inflammatoire pouvait limiter la progression des maladies hépatiques d'origine alcoolique ou non alcoolique.Afin de mener à bien ce projet, nous avons combiné l'utilisation de modèles murins de maladie hépatique d'origine alcoolique ou non alcoolique, des approches pharmacologiques et des expériences sur cellules isolées. Ces études ont été complétées par des données obtenues sur des biopsies humaines.Ce travail a permis de démontrer que favoriser la polarisation M2 des cellules de Küpffer protège le foie de la stéatose, de la mort hépatocytaire et de l'inflammation. Ces résultats identifient un nouveau mécanisme anti‐inflammatoire déclenché par les cellules de Küpffer polarisées M2 : l'induction sélective de l'apoptose des cellules de Küpffer polarisées M1. Ce travail ouvre de nouvelles perspectives à l'identification de stratégies pour limiter la progression des maladies hépatiques et pourrait également avoir des retombées plus larges dans le cadre d'autres maladies chroniques inflammatoires ciblant d'autres tissus que le… Advisors/Committee Members: Pavoine, Catherine (thesis director).

Subjects/Keywords: Alcool; Macrophages; Inflammation; Alcohol; Macrophages; Inflammation; 616.3

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Benkdane, M. (2012). Rôle protecteur des cellules de Küpffer de phénotype M2 anti-inflammatoire dans la maladie alcoolique du foie : Protective role of M2 anti-inflammatory Kupffer cells in alcoholic liver disease. (Doctoral Dissertation). Université Paris-Est. Retrieved from http://www.theses.fr/2012PEST0062

Chicago Manual of Style (16^th Edition):

Benkdane, Merieme. “Rôle protecteur des cellules de Küpffer de phénotype M2 anti-inflammatoire dans la maladie alcoolique du foie : Protective role of M2 anti-inflammatory Kupffer cells in alcoholic liver disease.” 2012. Doctoral Dissertation, Université Paris-Est. Accessed March 02, 2021. http://www.theses.fr/2012PEST0062.

MLA Handbook (7^th Edition):

Benkdane, Merieme. “Rôle protecteur des cellules de Küpffer de phénotype M2 anti-inflammatoire dans la maladie alcoolique du foie : Protective role of M2 anti-inflammatory Kupffer cells in alcoholic liver disease.” 2012. Web. 02 Mar 2021.

Vancouver:

Benkdane M. Rôle protecteur des cellules de Küpffer de phénotype M2 anti-inflammatoire dans la maladie alcoolique du foie : Protective role of M2 anti-inflammatory Kupffer cells in alcoholic liver disease. [Internet] [Doctoral dissertation]. Université Paris-Est; 2012. [cited 2021 Mar 02]. Available from: http://www.theses.fr/2012PEST0062.

Council of Science Editors:

Benkdane M. Rôle protecteur des cellules de Küpffer de phénotype M2 anti-inflammatoire dans la maladie alcoolique du foie : Protective role of M2 anti-inflammatory Kupffer cells in alcoholic liver disease. [Doctoral Dissertation]. Université Paris-Est; 2012. Available from: http://www.theses.fr/2012PEST0062

Texas A&M University

10. Kanameni, Srikanth. Transcriptional Profiling of Polarized Macrophages using RNA-Sequencing.

Degree: MS, Biomedical Sciences, 2015, Texas A&M University

URL: http://hdl.handle.net/1969.1/155022

► Adipose tissue macrophages (ATMs) are pivotal regulators for adipose tissue function, specifically contributing to the homeostasis of the adipose niche. Significantly increased ATMs and their… (more)

Subjects/Keywords: Macrophages; RNA-Sequencing

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kanameni, S. (2015). Transcriptional Profiling of Polarized Macrophages using RNA-Sequencing. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/155022

Chicago Manual of Style (16^th Edition):

Kanameni, Srikanth. “Transcriptional Profiling of Polarized Macrophages using RNA-Sequencing.” 2015. Masters Thesis, Texas A&M University. Accessed March 02, 2021. http://hdl.handle.net/1969.1/155022.

MLA Handbook (7^th Edition):

Kanameni, Srikanth. “Transcriptional Profiling of Polarized Macrophages using RNA-Sequencing.” 2015. Web. 02 Mar 2021.

Vancouver:

Kanameni S. Transcriptional Profiling of Polarized Macrophages using RNA-Sequencing. [Internet] [Masters thesis]. Texas A&M University; 2015. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1969.1/155022.

Council of Science Editors:

Kanameni S. Transcriptional Profiling of Polarized Macrophages using RNA-Sequencing. [Masters Thesis]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/155022

University of Manitoba

11. Mohammed, Ashfaque. SEMA3E REGULATES RESIDENT MACROPHAGES RESPONSE IN LIPOPOLYSACCHARIDE-INDUCED SEPSIS.

Degree: Immunology, 2016, University of Manitoba

URL: http://hdl.handle.net/1993/31616

► Sepsis is an overwhelming systemic inflammatory response to microbial infections. Macrophages are the key innate immune cells that provide the first line of defence against… (more)

▼ Sepsis is an overwhelming systemic inflammatory response to microbial infections. Macrophages are the key innate immune cells that provide the first line of defence against systemic infections during sepsis. Macrophages perform multiple functions during infections such as triggering inflammation, phagocytosis of microbes, and resolution of inflammation. So far, various molecules have been shown to be involved in the regulation of macrophages in inflammatory conditions. However, recently published studies suggest that Semaphorin3E (Sema3E) plays a pivotal role in the immune function of macrophages. The exact role of Sema3E associated with macrophages function in lipopolysaccharide (LPS) induced endotoxemia is unknown. To directly address the involvement of Sema3E in macrophages, we have used Sema3e gene deletion approaches in in vivo and cell-based setups. We found that Sema3e-/- mice displayed initial transient protection from LPS-induced hypothermia. Sema3e-/- mice showed lower inducible nitric oxide synthase (iNOS) expression in peritoneal macrophages without altering the integrity of TLR-4 after LPS injection. Sema3e-/- mice exhibit a lower level of tumour necrosis factor (TNF) and interleukin-6 (IL-6) in peritoneal lavage and serum as compared to wild type (WT) littermates. Bone marrow derived macrophages (BMDMs) from Sema3e-/- mice expressed low levels of pro-inflammatory cytokines and also exhibited significantly down-regulated phosphorylation of STAT3, ERK1/2, and NF-κB, upon LPS exposure. Overall, the current study provides direct evidence that the lack of Sema3E, makes macrophages to become less responsive to LPS by disturbing LPSIII initiated signaling transduction. These findings suggest that the inhibition of Sema3E might be a novel strategy to treat conditions triggered by the excessive production of inflammatory cytokines. Advisors/Committee Members: Gounni, Abdel Soussi (Immunology) (supervisor), Uzonna, Jude (Immunology) Keijzer, Richard (Surgery) (examiningcommittee).

Subjects/Keywords: Sema3E; Sepsis; Macrophages

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mohammed, A. (2016). SEMA3E REGULATES RESIDENT MACROPHAGES RESPONSE IN LIPOPOLYSACCHARIDE-INDUCED SEPSIS. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/31616

Chicago Manual of Style (16^th Edition):

Mohammed, Ashfaque. “SEMA3E REGULATES RESIDENT MACROPHAGES RESPONSE IN LIPOPOLYSACCHARIDE-INDUCED SEPSIS.” 2016. Masters Thesis, University of Manitoba. Accessed March 02, 2021. http://hdl.handle.net/1993/31616.

MLA Handbook (7^th Edition):

Mohammed, Ashfaque. “SEMA3E REGULATES RESIDENT MACROPHAGES RESPONSE IN LIPOPOLYSACCHARIDE-INDUCED SEPSIS.” 2016. Web. 02 Mar 2021.

Vancouver:

Mohammed A. SEMA3E REGULATES RESIDENT MACROPHAGES RESPONSE IN LIPOPOLYSACCHARIDE-INDUCED SEPSIS. [Internet] [Masters thesis]. University of Manitoba; 2016. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1993/31616.

Council of Science Editors:

Mohammed A. SEMA3E REGULATES RESIDENT MACROPHAGES RESPONSE IN LIPOPOLYSACCHARIDE-INDUCED SEPSIS. [Masters Thesis]. University of Manitoba; 2016. Available from: http://hdl.handle.net/1993/31616

University of Manchester

12. Belkot, Klaudyna Roza. The interactions between macrophages and fibroblasts in the context of cancer.

Degree: 2019, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:320561

► It has long been recognised that the formation of cancer associated fibroblasts (CAFs) is dictated by cancer cells. However, recent reports have suggested that the… (more)

▼ It has long been recognised that the formation of cancer associated fibroblasts (CAFs) is dictated by cancer cells. However, recent reports have suggested that the alterations in stromal cells, including fibroblasts, might precede the transformation of epithelial cells and act as a driver of the tumorigenesis. However, little is known about the mechanism underpinning the reprogramming of normal fibroblasts to CAFs without the involvement of cancer cells. Here, we have suggested that chronic inflammation could play a pivotal role in this process. Chronic inflammation has been linked with the origin of cancer for decades. It is estimated that approximately 20% of all cancer cases emerge as a direct consequence of long-lasting, â€˜smoulderingâ€™ inflammation. However, our knowledge about the exact mechanism(s) behind this vicious association remains elusive. Here, we have hypothesised that macrophages, the key orchestrators of chronic inflammation, could provoke the transformation of normal fibroblasts towards CAFs, in a similar manner as cancer cells do, and consequently create a favourable environment for malignant cells to arise, survive and then expand. To test our hypothesis, we have employed hTER-BJ1 fibroblasts and treated them with macrophage-conditioned media. Then, a series of experiments has been performed to assess whether these fibroblasts acquired the key characteristics of CAFs. Notably, we have suggested here for the first time that macrophages could trigger the reprogramming of normal fibroblasts towards CAF-like cells. More precisely, we have suggested that factors secreted by macrophages could provoke the acquisition of key features attributed to pro-tumourigenic CAFs, including the induction of oxidative stress, the metabolic switch from the mitochondrial oxidative phosphorylation to aerobic glycolysis, and the induction of autophagy and cellular senescence. All these processes, collectively, result in the formation of catabolic CAFs that produce and secrete energy-rich nutrients and regulatory factors that are known to support malignant cells. However, further experiments are required to explore whether these macrophage-activated fibroblasts (MAFs) alone are sufficient to prompt the malignant transformation of epithelial cells or whether the presence of MAFs acts as a catalyst that accelerates tumour formation when another carcinogen is co-present. Advisors/Committee Members: MONCADA, SALVADOR S, SAYAN, BERNA BS, Townsend, Paul, Moncada, Salvador, Sayan, Berna.

Subjects/Keywords: macrophages; fibroblasts; inflammation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Belkot, K. R. (2019). The interactions between macrophages and fibroblasts in the context of cancer. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:320561

Chicago Manual of Style (16^th Edition):

Belkot, Klaudyna Roza. “The interactions between macrophages and fibroblasts in the context of cancer.” 2019. Doctoral Dissertation, University of Manchester. Accessed March 02, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:320561.

MLA Handbook (7^th Edition):

Belkot, Klaudyna Roza. “The interactions between macrophages and fibroblasts in the context of cancer.” 2019. Web. 02 Mar 2021.

Vancouver:

Belkot KR. The interactions between macrophages and fibroblasts in the context of cancer. [Internet] [Doctoral dissertation]. University of Manchester; 2019. [cited 2021 Mar 02]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:320561.

Council of Science Editors:

Belkot KR. The interactions between macrophages and fibroblasts in the context of cancer. [Doctoral Dissertation]. University of Manchester; 2019. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:320561

University of Melbourne

13. CHUA, LIN LIN. Monocytes and macrophages in malaria infection: a phenotypic and functional analysis.

Degree: 2012, University of Melbourne

URL: http://hdl.handle.net/11343/37669

► Monocytes and macrophages (mono/macs) have been implicated in both protection and immunopathology in malaria; the latter is linked to excessive cytokine production, which has been… (more)

▼ Monocytes and macrophages (mono/macs) have been implicated in both protection and immunopathology in malaria; the latter is linked to excessive cytokine production, which has been associated with maternal anaemia and low birth weight (LBW) during malaria in pregnancy. To better understand the roles of mono/macs in malaria infection, a phenotypic and functional investigation was undertaken in the current study. Monocytes are heterogeneous and there is a subset of monocytes, characterised by CD16 expression, which are the main producers of pro-inflammatory cytokines. These CD16+ monocytes are present at low proportion in healthy individuals, but may be expanded during infection or inflammation. To understand how pregnancy may alter maternal monocytes and their responses to malaria, monocyte subsets in peripheral and placental blood from malaria-exposed but uninfected women in Papua New Guinea were first characterised. Pregnant women in this cohort expressed high proportions of pro-inflammatory CD16+ monocytes even without malaria infection and these were inversely correlated with maternal haemoglobin level and birth weight, suggesting a role for CD16+ monocytes in adverse clinical outcomes in pregnancy. Alterations to the proportion of CD16+ monocyte subset as a consequence of malaria infection need to be addressed in future study, given that the current study was limited by the low number of malaria-infected cases. Mono/macs can be activated by haemozoin (malaria pigment) and high levels of mono/macs that have phagocytosed haemozoin correlated with severe outcomes in malaria-infected children and non-pregnant adults. However, in this study, it was demonstrated that pigmented mono/mac density during gestation was not correlated with clinical outcomes at delivery, thus does not serve as a useful prognostic marker. In addition, a product of mono/mac activation, soluble CD163 (sCD163), was also investigated as a diagnostic marker for placental malaria. It was found that sCD163 levels were not a useful indicator of placental malaria, but higher levels of sCD163 inversely correlated with haemoglobin levels, implicating mono/mac activation in maternal anaemia. The importance of heterogeneities in parasite and macrophage populations in regulating cytokine production was also explored. Using an in vitro model of human monocyte-derived macrophages (MDMs), this study investigated how infected erythrocytes with placental-binding property (CS2 parasites) may differ from other parasite strain in activating macrophages to produce cytokines. CS2 parasites induced greater levels of pro-inflammatory cytokines compared to another parasite strain that binds CD36 (E8B parasites). In addition, to address the influence of macrophage heterogeneity on cytokine response, macrophages of different polarisation states were generated and stimulated with CS2 parasites. Macrophages generated using M-CSF and GM-CSF…

Subjects/Keywords: malaria monocytes macrophages

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

CHUA, L. L. (2012). Monocytes and macrophages in malaria infection: a phenotypic and functional analysis. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/37669

Chicago Manual of Style (16^th Edition):

CHUA, LIN LIN. “Monocytes and macrophages in malaria infection: a phenotypic and functional analysis.” 2012. Doctoral Dissertation, University of Melbourne. Accessed March 02, 2021. http://hdl.handle.net/11343/37669.

MLA Handbook (7^th Edition):

CHUA, LIN LIN. “Monocytes and macrophages in malaria infection: a phenotypic and functional analysis.” 2012. Web. 02 Mar 2021.

Vancouver:

CHUA LL. Monocytes and macrophages in malaria infection: a phenotypic and functional analysis. [Internet] [Doctoral dissertation]. University of Melbourne; 2012. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/11343/37669.

Council of Science Editors:

CHUA LL. Monocytes and macrophages in malaria infection: a phenotypic and functional analysis. [Doctoral Dissertation]. University of Melbourne; 2012. Available from: http://hdl.handle.net/11343/37669

University of Southern California

14. Margol, Ashley S. Presence of tumor associated macrophages in SHH medulloblastoma.

Degree: MS, Clinical, Biomedical and Translational Investigations, 2014, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/354987/rec/5211

► Purpose ❧ Medulloblastoma is the most common malignant brain tumor in pediatrics and is comprised of 4 subgroups, which differ histologically, molecularly and clinically. In… (more)

Subjects/Keywords: macrophages; medulloblastoma; TLDA

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Margol, A. S. (2014). Presence of tumor associated macrophages in SHH medulloblastoma. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/354987/rec/5211

Chicago Manual of Style (16^th Edition):

Margol, Ashley S. “Presence of tumor associated macrophages in SHH medulloblastoma.” 2014. Masters Thesis, University of Southern California. Accessed March 02, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/354987/rec/5211.

MLA Handbook (7^th Edition):

Margol, Ashley S. “Presence of tumor associated macrophages in SHH medulloblastoma.” 2014. Web. 02 Mar 2021.

Vancouver:

Margol AS. Presence of tumor associated macrophages in SHH medulloblastoma. [Internet] [Masters thesis]. University of Southern California; 2014. [cited 2021 Mar 02]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/354987/rec/5211.

Council of Science Editors:

Margol AS. Presence of tumor associated macrophages in SHH medulloblastoma. [Masters Thesis]. University of Southern California; 2014. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/354987/rec/5211

University of Manchester

15. Belkot, Klaudyna. The interactions between macrophages and fibroblasts in the context of cancer.

Degree: PhD, 2019, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/the-interactions-between-macrophages-and-fibroblasts-in-the-context-of-cancer(04e42f8d-a293-4d2e-b046-8003f0c39966).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.816311

► It has long been recognised that the formation of cancer associated fibroblasts (CAFs) is dictated by cancer cells. However, recent reports have suggested that the… (more)

▼ It has long been recognised that the formation of cancer associated fibroblasts (CAFs) is dictated by cancer cells. However, recent reports have suggested that the alterations in stromal cells, including fibroblasts, might precede the transformation of epithelial cells and act as a driver of the tumorigenesis. However, little is known about the mechanism underpinning the reprogramming of normal fibroblasts to CAFs without the involvement of cancer cells. Here, we have suggested that chronic inflammation could play a pivotal role in this process. Chronic inflammation has been linked with the origin of cancer for decades. It is estimated that approximately 20% of all cancer cases emerge as a direct consequence of long-lasting, 'smouldering' inflammation. However, our knowledge about the exact mechanism(s) behind this vicious association remains elusive. Here, we have hypothesised that macrophages, the key orchestrators of chronic inflammation, could provoke the transformation of normal fibroblasts towards CAFs, in a similar manner as cancer cells do, and consequently create a favourable environment for malignant cells to arise, survive and then expand. To test our hypothesis, we have employed hTER-BJ1 fibroblasts and treated them with macrophage-conditioned media. Then, a series of experiments has been performed to assess whether these fibroblasts acquired the key characteristics of CAFs. Notably, we have suggested here for the first time that macrophages could trigger the reprogramming of normal fibroblasts towards CAF-like cells. More precisely, we have suggested that factors secreted by macrophages could provoke the acquisition of key features attributed to pro-tumourigenic CAFs, including the induction of oxidative stress, the metabolic switch from the mitochondrial oxidative phosphorylation to aerobic glycolysis, and the induction of autophagy and cellular senescence. All these processes, collectively, result in the formation of catabolic CAFs that produce and secrete energy-rich nutrients and regulatory factors that are known to support malignant cells. However, further experiments are required to explore whether these macrophage-activated fibroblasts (MAFs) alone are sufficient to prompt the malignant transformation of epithelial cells or whether the presence of MAFs acts as a catalyst that accelerates tumour formation when another carcinogen is co-present.

Subjects/Keywords: inflammation; macrophages; fibroblasts

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Belkot, K. (2019). The interactions between macrophages and fibroblasts in the context of cancer. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/the-interactions-between-macrophages-and-fibroblasts-in-the-context-of-cancer(04e42f8d-a293-4d2e-b046-8003f0c39966).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.816311

Chicago Manual of Style (16^th Edition):

Belkot, Klaudyna. “The interactions between macrophages and fibroblasts in the context of cancer.” 2019. Doctoral Dissertation, University of Manchester. Accessed March 02, 2021. https://www.research.manchester.ac.uk/portal/en/theses/the-interactions-between-macrophages-and-fibroblasts-in-the-context-of-cancer(04e42f8d-a293-4d2e-b046-8003f0c39966).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.816311.

MLA Handbook (7^th Edition):

Belkot, Klaudyna. “The interactions between macrophages and fibroblasts in the context of cancer.” 2019. Web. 02 Mar 2021.

Vancouver:

Belkot K. The interactions between macrophages and fibroblasts in the context of cancer. [Internet] [Doctoral dissertation]. University of Manchester; 2019. [cited 2021 Mar 02]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-interactions-between-macrophages-and-fibroblasts-in-the-context-of-cancer(04e42f8d-a293-4d2e-b046-8003f0c39966).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.816311.

Council of Science Editors:

Belkot K. The interactions between macrophages and fibroblasts in the context of cancer. [Doctoral Dissertation]. University of Manchester; 2019. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-interactions-between-macrophages-and-fibroblasts-in-the-context-of-cancer(04e42f8d-a293-4d2e-b046-8003f0c39966).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.816311

Rutgers University

16. Francis, Mary. Mechanisms mediating macrophage accumulation and activation in the lung during the pathogenesis of ozone-induced lung injury.

Degree: PhD, Toxicology, 2017, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/53614/

► Classically and alternatively activated macrophages and inflammatory mediators they release play a key role in the pathogenesis of ozone-induced lung injury. In these studies, we… (more)

▼ Classically and alternatively activated macrophages and inflammatory mediators they release play a key role in the pathogenesis of ozone-induced lung injury. In these studies, we investigated the origin of these cells and mechanisms regulating their accumulation in the lung following ozone exposure. We hypothesized that macrophages originate in the bone marrow and the spleen, and that chemokine receptors CCR2 and CX3CR1 mediate their migration to the lung; moreover, macrophage activation is controlled, in part, by the nuclear receptor FXR. To test this hypothesis, we analyzed the effects of ozone on splenectomized mice, CCR2 knockout mice and FXR knockout mice. Following ozone exposure, increased numbers of pro-inflammatory CD11b+Ly6CHi and anti-inflammatory CD11b+Ly6CLo macrophages were observed in lungs of control (CTL) mice. Splenectomy resulted in decreases in pro-inflammatory macrophages in the lung and down regulation of CCR2, CCL2, and CCL4, but increases in CD11b+Ly6CLo anti-inflammatory macrophages. After ozone exposure, we also observed increases in lung macrophages staining positively for CCR2, a chemokine receptor known to mediate trafficking of pro-inflammatory macrophages from the bone marrow to sites of injury. Loss of CCR2 was associated with reduced numbers of CD11b+Ly6CHi and iNOS+ pro-inflammatory macrophages in the lung and decreased expression of the pro-inflammatory cytokines, IL-1β and TNFα. Decreases in proinflammatory/cytotoxic lung macrophages in SPX and CCR2-/- mice were correlated with reduced ozone toxicity and oxidative stress, demonstrating that these cells originate in both the spleen and bone marrow. To further investigate macrophage trafficking from the bone marrow, we generated GFP+ chimeric mice by adoptive transfer of 2x106 bone marrow (BM) cells from GFP+ mice into irradiated CTL mice. After 4 weeks, approximately 98% of BM cells were GFP+, while only 5% of lung macrophages were GFP+. Ozone exposure resulted in an increase in pro-inflammatory GFP+CD11b+Ly6CHi and anti-inflammatory GFP+CD11b+Ly6CLo macrophages in the lung at 24 h. Whereas GFP+Ly6CHi macrophages remained elevated for 72 h, increases in GFP+Ly6CLo macrophages were transient. These studies suggest that bone marrow contributes both pro- and anti-inflammatory macrophages to lung macrophage pools responding to ozone. This was confirmed using CX3CR1+/GFP reporter mice and by staining lung macrophages for CCR2. These data suggest that multiple macrophage subpopulations play distinct roles in ozone-induced lung injury. To investigate potential mechanisms regulating macrophage activation, we used transgenic mice lacking FXR, a nuclear receptor with anti-inflammatory activity. Treatment of WT mice with ozone resulted in increased FXR expression in the lung, most notably in macrophages. Loss of FXR resulted in increased numbers of pro-inflammatory Ly6CHi macrophages in the lung and prolonged up-regulation of iNOS, indicating chronic inflammation and macrophage activation. Conversely, numbers of MR+, YM1+, and Arg… Advisors/Committee Members: Laskin, Debra L (chair), Gerecke, Donald R (internal member), Laskin, Jeffrey D (internal member), Guo, Grace L (internal member), Zelikoff, Judity T (outside member).

Subjects/Keywords: Macrophages; Lungs – Pathophysiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Francis, M. (2017). Mechanisms mediating macrophage accumulation and activation in the lung during the pathogenesis of ozone-induced lung injury. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/53614/

Chicago Manual of Style (16^th Edition):

Francis, Mary. “Mechanisms mediating macrophage accumulation and activation in the lung during the pathogenesis of ozone-induced lung injury.” 2017. Doctoral Dissertation, Rutgers University. Accessed March 02, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/53614/.

MLA Handbook (7^th Edition):

Francis, Mary. “Mechanisms mediating macrophage accumulation and activation in the lung during the pathogenesis of ozone-induced lung injury.” 2017. Web. 02 Mar 2021.

Vancouver:

Francis M. Mechanisms mediating macrophage accumulation and activation in the lung during the pathogenesis of ozone-induced lung injury. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2021 Mar 02]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/53614/.

Council of Science Editors:

Francis M. Mechanisms mediating macrophage accumulation and activation in the lung during the pathogenesis of ozone-induced lung injury. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/53614/

17. Ramon RÃseo Paula Pessoa Bezerra de Menezes. Estudo da atividade enzimÃtica e dos efeitos do veneno da serpente Bothropoides insularis sobre macrÃfagos RAW 264.7 in vitro.

Degree: Master, 2013, Universidade Federal do Ceará

URL: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11372 ;

► Em todo o mundo, sÃo registrados mais de 3 milhÃes de acidentes envolvendo picadas de animais peÃonhentos por ano, das quais 125 a 150 mil… (more)

▼ Em todo o mundo, sÃo registrados mais de 3 milhÃes de acidentes envolvendo picadas de animais peÃonhentos por ano, das quais 125 a 150 mil culminam em Ãbito. No Brasil, a maioria dos casos ocorre com serpentes dos gÃneros Bothrops e Bothropoides, provocando uma grande variedade de complicaÃÃes locais e sistÃmicas, dentre os quais se destacam efeito mionecrÃtico, coagulaÃÃo intravascular disseminada, citotoxicidade, insuficiÃncia renal aguda e sepse. A serpente Bothropoides insularis Ã uma espÃcie nativa da Ilha de Queimada Grande, cujo veneno apresenta efeito tÃxico acentuado em diversos modelos experimentais. Entretanto, pouco Ã conhecido a respeito do efeito dessa peÃonha sobre cÃlulas com funÃÃo de defesa, nem o quanto esse efeito pode influenciar na toxicidade observada in vivo. O presente trabalho teve como objetivo investigar as alteraÃÃes celulares induzidas pelo veneno total da serpente Bothropoides insularis (BinsVT) sobre macrÃfagos murinos da linhagem RAW 264.7. Nesse contexto, foi realizada a determinaÃÃo da atividade proteolÃtica e da produÃÃo de perÃxido de hidrogÃnio in vitro de BinsVT atravÃs de reaÃÃes colorimÃtricas. Os resultados demonstraram alta atividade catalÃtica em ambos os testes, sugerindo que os efeitos biolÃgicos desse veneno podem estar relacionados Ã presenÃa de enzimas como metaloproteinases (svMPs) e L-aminoÃcido oxidases (LAAOs) em concentraÃÃes relevantes nas condiÃÃes experimentais adotadas. A determinaÃÃo do potencial citotÃxico foi realizada pelo mÃtodo de reduÃÃo do MTT, um teste de avaliaÃÃo da capacidade oxirredutora das cÃlulas, apÃs 2, 6, 12 e 24 horas de incubaÃÃo. Foi observado efeito citotÃxico em altas concentraÃÃes de forma tempo-dependente, com morte celular mais pronunciada nas concentraÃÃes de 200 e 100 Âg/mL apÃs 12 e 24 horas de tratamento. Nas menores concentraÃÃes estudadas, ocorreu um aumento gradativo da viabilidade celular, com valores percentuais em torno de 200% em relaÃÃo ao grupo controle nos grupos tratados por 24 horas. Esse resultado sugere a presenÃa de efeito proliferativo de BinsVT sobre essa linhagem celular. Em seguida, a atividade da enzima lactato desidrogenase (LDH) no sobrenadante de cultivo dos grupos experimentais foi determinado para investigaÃÃo de lise celular induzida por BinsVT. Foi verificado aumento significativo da atividade dessa enzima em todos os grupos testados, sugerindo a coexistÃncia de fraÃÃes com efeito proliferativo e citotÃxico, e a concentraÃÃo e o tempo de exposiÃÃo do veneno determinam qual irÃ prevalecer. Para avaliaÃÃo morfolÃgica das cÃlulas RAW 264.7 apÃs exposiÃÃo Ã substÃncia em estudo, os experimentos foram realizados na superfÃcie de lamÃnulas, para coloraÃÃo com May-Grunwald Giemsa. Os grupos experimentais foram analisados por microscopia Ãptica e as caracterÃsticas morfolÃgicas mais representativas foram fotomicrografadas. Foram observadas diversas alteraÃÃes morfolÃgicas, tais como aparecimento de fragmentos celulares e nÃcleos desnudos, cÃlulas vacuolizadas, reduÃÃo do volume celular e aumento de projeÃÃes… Advisors/Committee Members: JanaÃna Serra Azul Monteiro Evangelista, Alice Maria Costa Martins, ArlÃndia Cristina Lima Nobre de Morais.

Subjects/Keywords: FARMACOLOGIA; MacrÃfagos; Citotoxinas; Macrophages; Cytotoxins

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Menezes, R. R. P. P. B. d. (2013). Estudo da atividade enzimÃtica e dos efeitos do veneno da serpente Bothropoides insularis sobre macrÃfagos RAW 264.7 in vitro. (Masters Thesis). Universidade Federal do Ceará. Retrieved from http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11372 ;

Chicago Manual of Style (16^th Edition):

Menezes, Ramon RÃseo Paula Pessoa Bezerra de. “Estudo da atividade enzimÃtica e dos efeitos do veneno da serpente Bothropoides insularis sobre macrÃfagos RAW 264.7 in vitro.” 2013. Masters Thesis, Universidade Federal do Ceará. Accessed March 02, 2021. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11372 ;.

MLA Handbook (7^th Edition):

Menezes, Ramon RÃseo Paula Pessoa Bezerra de. “Estudo da atividade enzimÃtica e dos efeitos do veneno da serpente Bothropoides insularis sobre macrÃfagos RAW 264.7 in vitro.” 2013. Web. 02 Mar 2021.

Vancouver:

Menezes RRPPBd. Estudo da atividade enzimÃtica e dos efeitos do veneno da serpente Bothropoides insularis sobre macrÃfagos RAW 264.7 in vitro. [Internet] [Masters thesis]. Universidade Federal do Ceará 2013. [cited 2021 Mar 02]. Available from: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11372 ;.

Council of Science Editors:

Menezes RRPPBd. Estudo da atividade enzimÃtica e dos efeitos do veneno da serpente Bothropoides insularis sobre macrÃfagos RAW 264.7 in vitro. [Masters Thesis]. Universidade Federal do Ceará 2013. Available from: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11372 ;

Université du Québec à Montréal

18. Warburton, Christopher. Les macrophages stimulent la production de proérythroblastes et la différentiation érythrocytaire par contact direct en absence d'EPO exogène.

Degree: 2017, Université du Québec à Montréal

URL: http://www.archipel.uqam.ca/9833/1/M15016.pdf

► L'érythropoïèse est principalement régulée par l'hormone rénale érythropoïétine (EPO), qui stimule la prolifération et la différentiation des précurseurs érythropoïétiques à travers des effets anti-apoptotiques et… (more)

▼ L'érythropoïèse est principalement régulée par l'hormone rénale érythropoïétine (EPO), qui stimule la prolifération et la différentiation des précurseurs érythropoïétiques à travers des effets anti-apoptotiques et antioxydants. Sous des conditions homéostatiques, les érythroblastes de la moelle osseuse s'organisent en ilots autour d'un macrophage central, qui supporte l'échange de fer nécessaire à la synthèse d'hémoglobine ainsi que la phagocytose de noyaux extrudés. Le fait que la déplétion expérimentale in vivo de macrophages cause une déficience rapide de l'érythropoïèse nous a mené à émettre l'hypothèse que les macrophages peuvent être une source d'EPO in situ, ou produisent des analogues fonctionnels à l'EPO. Afin de valider cette hypothèse, la contribution des facteurs solubles dérivés des macrophages de la moelle osseuse ainsi que l'impact d'interaction cellulaire directe ace des précurseurs hématopoïétiques ont été étudié in vitro dans des conditions de culture sans EPO. Des cellules lignées négative de la moelle osseuse, enrichies par sélection négative, ont étés mises en culture en présence de milieu conditionné par les macrophages dérivés de la moelle osseuse (BMDM), ou en contact direct avec ceux-ci, dans un milieu contenant de l'insuline humaine, de l'holotransferrine et d'albumine bovine dé-ionisée mais exempte d'EPO. L'impact de la déplétion in vivo des macrophages sur l'érythropoïèse a été étudié en injectant des liposomes de Clodronate dans des souris Balb/c. Les populations érythrocytaires ont étés analysés ex vivo par FACS en utilisant des anticorps anti-CD71 et Ter119, ou par coloration May-Grünwald et Giemsa. Nos résultats démontrent que le milieu conditionné de BMDM promeut la différentiation des stades précoces érythrocytaires (proérythroblastes) et diminue la prolifération des stades tardifs érythrocytaires. La déplétion des macrophages pendant une semaine cause un arrêt complet de l'érythropoïèse dans la moelle osseuse sans toutefois induire une production compensatoire d'EPO par le rein. L'EPO n'as pu être détectée par PCR, Western Blot ou ELISA dans les surnageant et les lysats de BMDM en condition de culture normoxique et hypoxique. Ces résultats démontrent qu'en condition expérimentale sans ajout d'EPO exogène, les macrophages de la moelle osseuse stimulent les phases précoces de différentiation érythrocytaire.

Subjects/Keywords: Érythropoïèse – Régulation; Érythropoïétine; Macrophages

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Warburton, C. (2017). Les macrophages stimulent la production de proérythroblastes et la différentiation érythrocytaire par contact direct en absence d'EPO exogène. (Thesis). Université du Québec à Montréal. Retrieved from http://www.archipel.uqam.ca/9833/1/M15016.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Warburton, Christopher. “Les macrophages stimulent la production de proérythroblastes et la différentiation érythrocytaire par contact direct en absence d'EPO exogène.” 2017. Thesis, Université du Québec à Montréal. Accessed March 02, 2021. http://www.archipel.uqam.ca/9833/1/M15016.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Warburton, Christopher. “Les macrophages stimulent la production de proérythroblastes et la différentiation érythrocytaire par contact direct en absence d'EPO exogène.” 2017. Web. 02 Mar 2021.

Vancouver:

Warburton C. Les macrophages stimulent la production de proérythroblastes et la différentiation érythrocytaire par contact direct en absence d'EPO exogène. [Internet] [Thesis]. Université du Québec à Montréal; 2017. [cited 2021 Mar 02]. Available from: http://www.archipel.uqam.ca/9833/1/M15016.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Warburton C. Les macrophages stimulent la production de proérythroblastes et la différentiation érythrocytaire par contact direct en absence d'EPO exogène. [Thesis]. Université du Québec à Montréal; 2017. Available from: http://www.archipel.uqam.ca/9833/1/M15016.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of California – Merced

19. Premasekharan, Gayatri. Inflammatory mechanism induced by natural and engineered silica particles in human-derived macrophages at low non-cytotoxic doses.

Degree: Biological and Small-scale Technologies, 2012, University of California – Merced

URL: http://www.escholarship.org/uc/item/2jr9r8hf

► Particle size, phase, and transition metals have all been implicated in natural and engineered silica-induced respiratory effects, as well as cellular interactions. However, efforts to… (more)

▼ Particle size, phase, and transition metals have all been implicated in natural and engineered silica-induced respiratory effects, as well as cellular interactions. However, efforts to unambiguously determine their role in the pro-inflammatory mechanism induction have been hampered due to the use of inhomogeneous samples, with incomplete characterization and the use of high cytotoxic doses. Here, engineered micro- and nano- sized silica particles, which are more homogenous in their materials properties and used in a variety of applications, were characterized and compared to natural silica at a realistic dose level. Natural (2 μm) and engineered silica particles (2 μm and 50 nm) were characterized and controlled for size, morphology, phase, iron presence, surface area, and aggregation. A novel lipid peroxidation-dependent pro-inflammatory mechanism due to the influence of iron, particle size, and phase was hypothesized for these particles under a low non-cytotoxic dose closer to a realistic exposure regime. It was observed that at a 1 μg/ml low non-cytotoxic dose of silica the presence or addition of iron, reduction of particle size, and crystalline phase of natural silica significantly increased superoxide (O2.-) and hydrogen peroxide (H2O2) production in the macrophages. This increase in O2.- and H2O2 production, further lead to phosphatidylcholine-specific phospholipase C (PC-PLC) - mediated inflammatory mediator or cytokine production in macrophages via lipid peroxidation and lipid raft disruption (large fraction sub-domains of plasma membrane involved in signal transduction). Addition of an iron chelator abrogated these responses, supporting the role of iron in the hypothesized mechanism. Activation of PC-PLC - induced inflammatory response was determined by using PC-PLC inhibitor, Tricychodecan-9-yl-xanthate, which blocked the inflammatory mediator production. Microscopy studies with cell-particle interaction revealed that particle size also influenced the uptake of silica particles in the macrophages mainly via phagocytosis, since binding and activation of membrane receptors and subsequent internalization is strongly dependent on nanoparticle size. Also, a high cytotoxic dose of 100 μg/ml showed macrophage particle overload for both particle sizes, with macrophage damage possibly leading to catastrophic release of inflammatory mediators that could obfuscate study of the normal inflammatory response, emphasizing the need for studies with realistic exposure doses. In summary, this work demonstrated the role of particle size, iron, and phase in a lipid raft dependent-inflammatory mechanism induced by particles at a realistic exposure dose via PC-PLC. It should lead to a better understanding of the mechanism and important parameters for the particle-induced inflammatory response of the lungs, and therefore, control of the respiratory effects caused by real-life exposure to natural and engineered particles.

Subjects/Keywords: Biology.; silica; macrophages; inflammatory mechanism

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Premasekharan, G. (2012). Inflammatory mechanism induced by natural and engineered silica particles in human-derived macrophages at low non-cytotoxic doses. (Thesis). University of California – Merced. Retrieved from http://www.escholarship.org/uc/item/2jr9r8hf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Premasekharan, Gayatri. “Inflammatory mechanism induced by natural and engineered silica particles in human-derived macrophages at low non-cytotoxic doses.” 2012. Thesis, University of California – Merced. Accessed March 02, 2021. http://www.escholarship.org/uc/item/2jr9r8hf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Premasekharan, Gayatri. “Inflammatory mechanism induced by natural and engineered silica particles in human-derived macrophages at low non-cytotoxic doses.” 2012. Web. 02 Mar 2021.

Vancouver:

Premasekharan G. Inflammatory mechanism induced by natural and engineered silica particles in human-derived macrophages at low non-cytotoxic doses. [Internet] [Thesis]. University of California – Merced; 2012. [cited 2021 Mar 02]. Available from: http://www.escholarship.org/uc/item/2jr9r8hf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Premasekharan G. Inflammatory mechanism induced by natural and engineered silica particles in human-derived macrophages at low non-cytotoxic doses. [Thesis]. University of California – Merced; 2012. Available from: http://www.escholarship.org/uc/item/2jr9r8hf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Tulane University

20. Delery, Elizabeth. Choroid Plexus in AIDS Pathogenesis.

Degree: 2019, Tulane University

URL: https://digitallibrary.tulane.edu/islandora/object/tulane:94533

►

[email protected]

The prevalence of HIV-associated neurocognitive disorders (HAND) has increased in the era of combination anti-retroviral therapy (cART). Despite this and documented neurocognitive impairment, there… (more)

▼

[email protected]

The prevalence of HIV-associated neurocognitive disorders (HAND) has increased in the era of combination anti-retroviral therapy (cART). Despite this and documented neurocognitive impairment, there is a lack of pathology of HIV-encephalitis (HIVE), specifically multi-nucleated giant cells (MNGCs), in children and SIV-encephalitis (SIVE) in rhesus macaques infected pre-, peri-, and post-parturition. In this dissertation, we show that the lack of MNGCs seen is most likely due to innate differences in the blood-brain and blood-CSF barriers, and a robust pro- and anti-inflammatory response in neonatal rhesus macaques. Using a rhesus macaque model of HIV, we examined the plasma viral load, brain tissue viral load, and monocyte turnover, using PCR and flow cytometry, respectively. We also performed immunohistochemistry for monocyte, macrophage, tight junction, and aging markers of the choroid plexus. We sought to create a choroid plexus epithelial cell model to monitor the effects of inflammatory markers and virus on the tight junctions of the blood-CSF barrier in real-time. We demonstrated that neonates do not develop encephalitis, despite comparable viral load and monocyte turnover, previously established correlates of SIV-encephalitis (SIVE). However, we noted that uninfected adult rhesus macaques have an increase in virus susceptible cells in the brain, SIV-infected adults have a leakier blood-brain barrier than infected neonates, and adults with encephalitis have a greater viral burden in brain tissue compared to adults without encephalitis. In the choroid plexus, we discovered that despite the lack of encephalitis, neonates have an increase in monocytes and macrophages of the choroid plexus, indicating a strong immune response. While our choroid plexus epithelial cell model is still in preliminary stages, initial results are promising. Our work indicates a possible viral threshold needed for the development of encephalitis, and that the blood-brain barrier may play a role in this threshold due to lower levels of virus susceptible cells and a tighter blood brain barrier in neonates. In the choroid plexus, the strong pro- and anti-inflammatory macrophage response seen in neonates may offer an extra layer of protection development of SIVE. Our data also indicates that SIV causes a marked decrease in the expression of klotho, the anti-aging hormone that is produced in high levels in the choroid plexus in the brain. This could potentially explain the premature inflammaging phenotype seen in chronic infections.

1

Elizabeth Delery

Advisors/Committee Members: MacLean, Andrew (Thesis advisor), School of Medicine Biomedical Sciences Graduate Program (Degree granting institution).

Subjects/Keywords: Choroid Plexus; HIV; Macrophages

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Delery, E. (2019). Choroid Plexus in AIDS Pathogenesis. (Thesis). Tulane University. Retrieved from https://digitallibrary.tulane.edu/islandora/object/tulane:94533

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Delery, Elizabeth. “Choroid Plexus in AIDS Pathogenesis.” 2019. Thesis, Tulane University. Accessed March 02, 2021. https://digitallibrary.tulane.edu/islandora/object/tulane:94533.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Delery, Elizabeth. “Choroid Plexus in AIDS Pathogenesis.” 2019. Web. 02 Mar 2021.

Vancouver:

Delery E. Choroid Plexus in AIDS Pathogenesis. [Internet] [Thesis]. Tulane University; 2019. [cited 2021 Mar 02]. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:94533.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Delery E. Choroid Plexus in AIDS Pathogenesis. [Thesis]. Tulane University; 2019. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:94533

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Rochester

21. Amie, Sarah M.; Kim, Baek. Replication of HIV in macrophages : effects of SAMHD1 on dNTP Levels, viral mutagenesis, and antiviral efficacy.

Degree: PhD, 2014, University of Rochester

URL: http://hdl.handle.net/1802/28455

► Lentiviruses such as HIV are unique in that they replicate in both dividing CD4+ T cells and non-dividing macrophages. Activated CD4+ T cells progress through… (more)

▼ Lentiviruses such as HIV are unique in that they replicate in both dividing CD4+ T cells and non-dividing macrophages. Activated CD4+ T cells progress through S phase and have an abundant amount of dNTPs to replicate genomic DNA, whereas macrophages remain in the resting phase and do not require high levels of dNTPs. Another factor that maintains low dNTP levels in macrophages is a protein called SAM domain and HD domain-containing protein 1 (SAMHD1), which hydrolyzes dNTPs into dNs. SAMHD1 was previously characterized as a dGTP dependent triphosphohydrolase, but with several assays in vitro we have shown that the ribonucleotide GTP is the primary allosteric activator. SAMHD1 is an antiretroviral host factor that restricts viral replication by limiting the dNTP substrate availability for reverse transcriptase (RT). HIV-2 counteracts SAMHD1 by expressing an accessory protein vpx, which targets it for proteasomal degradation. This results in an increase in cellular dNTPs and rapid completion of viral DNA synthesis. However, HIV-1 does not employ a mechanism to degrade SAMHD1, and therefore replicates, although at low levels, even with the limited dNTPs found in macrophages. SAMHD1 is specific for dNTPs and is not able to hydrolyze rNTPs; therefore the concentration of rNTPs is in the millimolar range in both dividing and non-dividing cell types such that RNA polymerases can continuously synthesize RNA. This creates a large disparity between dNTPs and rNTPs, particularly in macrophages, during HIV-1 replication. Consequently, HIV-1 RT frequently incorporates rNMPs in the viral genome possibly contributing to the high mutation rate of HIV-1. SAMHD1 also selects dNTPs over the triphosphate form of nucleoside reverse transcriptase inhibitors (NRTI-TPs), which are analogous in structure to cellular dNTPs, but lack a 3' OH group on the ribose moiety. Although SAMHD1 does not decrease the concentration of NRTI-TPs by direct hydrolysis, degradation of SAMHD1 in macrophages significantly reduces drug efficacy. This is caused by the increase in cellular dNTPs upon degradation of SAMHD1, which out compete NRTI-TPs for the active site of RT. These findings suggest that NRTI-TPs are not as effective at inhibiting HIV-2 as they are at inhibiting HIV-1 infection in macrophages.

Subjects/Keywords: HIV; SAMHD1; dNTPs; Macrophages

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Amie, Sarah M.; Kim, B. (2014). Replication of HIV in macrophages : effects of SAMHD1 on dNTP Levels, viral mutagenesis, and antiviral efficacy. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/28455

Chicago Manual of Style (16^th Edition):

Amie, Sarah M.; Kim, Baek. “Replication of HIV in macrophages : effects of SAMHD1 on dNTP Levels, viral mutagenesis, and antiviral efficacy.” 2014. Doctoral Dissertation, University of Rochester. Accessed March 02, 2021. http://hdl.handle.net/1802/28455.

MLA Handbook (7^th Edition):

Amie, Sarah M.; Kim, Baek. “Replication of HIV in macrophages : effects of SAMHD1 on dNTP Levels, viral mutagenesis, and antiviral efficacy.” 2014. Web. 02 Mar 2021.

Vancouver:

Amie, Sarah M.; Kim B. Replication of HIV in macrophages : effects of SAMHD1 on dNTP Levels, viral mutagenesis, and antiviral efficacy. [Internet] [Doctoral dissertation]. University of Rochester; 2014. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1802/28455.

Council of Science Editors:

Amie, Sarah M.; Kim B. Replication of HIV in macrophages : effects of SAMHD1 on dNTP Levels, viral mutagenesis, and antiviral efficacy. [Doctoral Dissertation]. University of Rochester; 2014. Available from: http://hdl.handle.net/1802/28455

Rochester Institute of Technology

22. Malinski, Lorri Jean. Determination of the neighboring molecule to the FC receptor on human macrophages.

Degree: School of Chemistry and Materials Science (COS), 1984, Rochester Institute of Technology

URL: https://scholarworks.rit.edu/theses/556

► Chemical cross-linking studies have been carried out to investigate near neighbors to the receptor for immunoglobulin G[lgG] on U937 cells both before and after solubilization… (more)

Subjects/Keywords: Macrophages; Immunoglobulins

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APA (6^th Edition):

Malinski, L. J. (1984). Determination of the neighboring molecule to the FC receptor on human macrophages. (Thesis). Rochester Institute of Technology. Retrieved from https://scholarworks.rit.edu/theses/556

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Malinski, Lorri Jean. “Determination of the neighboring molecule to the FC receptor on human macrophages.” 1984. Thesis, Rochester Institute of Technology. Accessed March 02, 2021. https://scholarworks.rit.edu/theses/556.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Malinski, Lorri Jean. “Determination of the neighboring molecule to the FC receptor on human macrophages.” 1984. Web. 02 Mar 2021.

Vancouver:

Malinski LJ. Determination of the neighboring molecule to the FC receptor on human macrophages. [Internet] [Thesis]. Rochester Institute of Technology; 1984. [cited 2021 Mar 02]. Available from: https://scholarworks.rit.edu/theses/556.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Malinski LJ. Determination of the neighboring molecule to the FC receptor on human macrophages. [Thesis]. Rochester Institute of Technology; 1984. Available from: https://scholarworks.rit.edu/theses/556

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Alberta

23. Al-Hallak, MHD Kamal. Inhalable nanoparticles in lung cancer treatment; efficacy, safety, distribution and nanoparticle-macrophage interactions.

Degree: PhD, Faculty of Pharmacy and Pharmaceutical Sciences, 2012, University of Alberta

URL: https://era.library.ualberta.ca/files/mk61rj53p

► In 2002, lung cancer was responsible for 17.6% of the total worldwide deaths from cancer. Beyond the three traditional forms of cancer treatment, surgery, radiation… (more)

▼ In 2002, lung cancer was responsible for 17.6% of the total worldwide deaths from cancer. Beyond the three traditional forms of cancer treatment, surgery, radiation therapy, and chemotherapy, targeted drug delivery therapy has shown to be a potential treatment option. The design of a successful delivery system requires consideration of many factors, some of which include (i) the location and main organ(s) affected; (ii) the complexity of the associated physiological changes; (iii) the changes in receptor expression in cancerous cells; (iv) the physiochemical properties of the delivery system; (v) the interactions between the cancerous cells and other adjuvant cells, such as macrophages, with the delivery system; and (vi) the safety and tolerability of the delivery system. Considering the above factors of a successful delivery system, the aim of the present work was to design an innovative delivery system for lung cancer treatment incorporating inhalable nanoparticles (NP). To achieve this goal, several objectives were developed: (i) to investigate the interactions of different NP formulations with macrophages and the resulting effects on the behavior of macrophages; (ii) to assess and correlate the pulmonary toxicity of inhalable NPs using in vivo and in vitro methods; (iii) to develop a method to assess in real-time the effect of the formulation modifications on the uptake by macrophages of NPs; (iv) to assess the in vivo efficacy of an innovative formulation of effervescent inhalable NPs, thus actively releasing NPs; and finally, (v) to investigate the distribution of effervescent inhalable NPs after pulmonary delivery. Our results demonstrate that after exposure to NPs, macrophages undergo cellular changes to gain the ability to produce Th1 cytokines that are able to affect the viability of cancerous cells. The tolerability of inhalable NPs was related mainly to the additives used in the NP formulation. There was a good correlation between the in vivo and in vitro results. Effervescent inhalable NPs proved to be an effective and tolerable treatment for lung cancer treatment. Whole body autoradiography showed that inhalable NPs were able to achieve deep lung deposition and become distributed in time over the whole lung with some extra-pulmonary distribution.

Subjects/Keywords: inhalable nanoparticles; Lung cancer; Macrophages

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APA (6^th Edition):

Al-Hallak, M. K. (2012). Inhalable nanoparticles in lung cancer treatment; efficacy, safety, distribution and nanoparticle-macrophage interactions. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/mk61rj53p

Chicago Manual of Style (16^th Edition):

Al-Hallak, MHD Kamal. “Inhalable nanoparticles in lung cancer treatment; efficacy, safety, distribution and nanoparticle-macrophage interactions.” 2012. Doctoral Dissertation, University of Alberta. Accessed March 02, 2021. https://era.library.ualberta.ca/files/mk61rj53p.

MLA Handbook (7^th Edition):

Al-Hallak, MHD Kamal. “Inhalable nanoparticles in lung cancer treatment; efficacy, safety, distribution and nanoparticle-macrophage interactions.” 2012. Web. 02 Mar 2021.

Vancouver:

Al-Hallak MK. Inhalable nanoparticles in lung cancer treatment; efficacy, safety, distribution and nanoparticle-macrophage interactions. [Internet] [Doctoral dissertation]. University of Alberta; 2012. [cited 2021 Mar 02]. Available from: https://era.library.ualberta.ca/files/mk61rj53p.

Council of Science Editors:

Al-Hallak MK. Inhalable nanoparticles in lung cancer treatment; efficacy, safety, distribution and nanoparticle-macrophage interactions. [Doctoral Dissertation]. University of Alberta; 2012. Available from: https://era.library.ualberta.ca/files/mk61rj53p

Cornell University

24. Xue, Zhen. The Physiological Function And Regulatory Mechanisms Of The Unfolded Protein Response And Endoplasmic Reticulum Associated Degradation.

Degree: PhD, Nutrition, 2014, Cornell University

URL: http://hdl.handle.net/1813/36201

► ER protein homeostasis plays an important role in normal organism physiological and pathological conditions. ER stress induces activation of the unfolded protein response, which reacts… (more)

▼ ER protein homeostasis plays an important role in normal organism physiological and pathological conditions. ER stress induces activation of the unfolded protein response, which reacts to reset ER homeostasis by enhancing protein folding capacity, reducing protein translation load and up-regulating ER associated degradation. It is important to understand the physiological role of each main UPR or ERAD component as well as their molecular regulatory mechanisms. IRE1[alpha], the most conserved UPR sensor protein, is a bifunctional enzyme containing both a kinase and RNase domain that are important for transautophosphorylation and Xbp1 mRNA splicing, respectively. However, the amino acid residues important for structural integrity remain largely unknown. This research has identified a highly conserved proline residue at position 830 (P830) that is critical for IRE1[alpha] structural integrity, hence the activation of both kinase and RNase domains. Further structural analysis reveals that P830 could form a highly conserved structural linker with adjacent tryptophan and tyrosine residues at positions 833 and 945 (W833 and Y945) thereby bridging the kinase and RNase domains. This finding may facilitate the identification of small molecules which specifically compromise IRE1[alpha] function. Previously, ER stress has been shown to activate inflammatory responses. Yet, whether this is true with ERAD in vivo remains to be demonstrated. Using macrophage-specific Sel1L (a key protein component of the Sel1L-Hrd1 ERAD complex) knock-out mice, our data challenges the causal link between ER stress and inflammation in a physiological setting. This research shows that Sel1L is dispensable for normal macrophage innate immunity functions. Although these macrophages exhibited elevated protein levels of a subset of ER chaperones and dilated ER cisternae at the basal conditions, surprisingly these changes are uncoupled from macrophage antigen presenting function, cytokine secretion function, and inflammatory responses against bacterial pathogens as well as in obese adipose tissues. Thus, we conclude that physiological mild ER stress may not play a causal role in inflammation in macrophages. ii Advisors/Committee Members: Qi, Ling (chair), Long, Qiaoming (committee member), Lee, Siu Sylvia (committee member), Stipanuk, Martha Harney (committee member).

Subjects/Keywords: IRE1alpha; ER Associated Degradation; macrophages

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APA (6^th Edition):

Xue, Z. (2014). The Physiological Function And Regulatory Mechanisms Of The Unfolded Protein Response And Endoplasmic Reticulum Associated Degradation. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/36201

Chicago Manual of Style (16^th Edition):

Xue, Zhen. “The Physiological Function And Regulatory Mechanisms Of The Unfolded Protein Response And Endoplasmic Reticulum Associated Degradation.” 2014. Doctoral Dissertation, Cornell University. Accessed March 02, 2021. http://hdl.handle.net/1813/36201.

MLA Handbook (7^th Edition):

Xue, Zhen. “The Physiological Function And Regulatory Mechanisms Of The Unfolded Protein Response And Endoplasmic Reticulum Associated Degradation.” 2014. Web. 02 Mar 2021.

Vancouver:

Xue Z. The Physiological Function And Regulatory Mechanisms Of The Unfolded Protein Response And Endoplasmic Reticulum Associated Degradation. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1813/36201.

Council of Science Editors:

Xue Z. The Physiological Function And Regulatory Mechanisms Of The Unfolded Protein Response And Endoplasmic Reticulum Associated Degradation. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/36201

University of Saskatchewan

25. Darbellay, Joseph Andikpeme 1989-. Elucidating the Role of Antigen-presenting Cells in the Immunopathogenesis of the Porcine Reproductive and Respiratory Syndrome Virus.

Degree: 2019, University of Saskatchewan

URL: http://hdl.handle.net/10388/12149

► The porcine reproductive and respiratory syndrome virus (PRRSV) is a positive sense single-stranded RNA virus of the arteriviridae family and is one of the most… (more)

▼ The porcine reproductive and respiratory syndrome virus (PRRSV) is a positive sense single-stranded RNA virus of the arteriviridae family and is one of the most economically devastating pathogens in the swine industry today. The PRRSV was discovered in the early 1990s in Europe and the United States, with strains being divided into Type 1 and Type 2 genotypes, respectively. Disease outcomes range from being asymptomatic to upwards of 100% mortality in herds, being attributable to the pathogenicity of the PRRSV strain, to co-infections with opportunistic pathogens, and to the age and breed of the pig. Animals subject to infection with PRRSV exhibit an array of clinical symptoms, including but not limited to, respiratory difficulty and pneumonia, weight loss, immune suppression leading to secondary bacterial infections, and spontaneous abortions/fetal mummification, from which the majority of the economic losses stem. Immunization with modified live vaccines are the most popular intervention to control disease, and although they are effective in improving health status of animals, the currently distributed vaccines pose a risk of reversion to virulence and afford limited cross protection amongst circulating strains of the virus. Thus, there is a high demand for a safe and effective vaccine. The goal of this study was to investigate the role of specific antigen-presenting cell (APC) subsets during the pathogenesis of PRRSV and to further understand the progression to T cell immunity in response to PRRSV. To accomplish this, we chose to investigate the susceptibility of bone marrow-derived dendritic cells (BMDCs), monocyte-derived dendritic cells (MoDCs), and monocyte-derived macrophages (MoMΦs). After successfully differentiating and characterizing BMDCs from hematopoietic stem cells isolated from the sternum of animals, we demonstrated that PRRSV infection is restricted only to APCs that express CD163. Furthermore, we showed that PRRSV replicates more quickly in MoMΦ cell cultures than in CD163+ BMDC cultures and potentially in MoDCs. We continued to investigate PRRSV infection of APCs and discovered that in non-infected MoDCs, the cellular protein gamma actin 1 associates closely with MHCII. When MoDCs were infected with PRRSV, gamma actin 1 was no longer associated with MHCII. We hypothesize that PRRSV could be manipulating the actin cytoskeleton, potentially interfering with MHCII peptide presentation. Ultimately, we were interested in the interaction of APCs with T cells. In order to study this interaction, we developed an assay utilizing a mixed leukocyte reaction (MLR). Our hypothesis was confirmed in the MLR that showed M1 MoMΦs (IFN-γ stimulated) are more potent inducers of cytotoxic lymphocyte (CTLs) and CD4α+ T cell proliferation than M2 MoMΦs (IL-4 stimulated) or M0 MoMΦs (non-stimulated). In addition, our results indicated that gamma delta (γδ) T cells did not participate in the MLR. Next we proceeded with an animal trial investigating the interaction of APCs with T cells in a PRRSV-antigen specific… Advisors/Committee Members: Gerdts, Volker, Meurens, Francois, Gordon, John, Tikoo, Suresh, Hill, Janet.

Subjects/Keywords: PRRSV; Dendritic cells; Macrophages

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APA (6^th Edition):

Darbellay, J. A. 1. (2019). Elucidating the Role of Antigen-presenting Cells in the Immunopathogenesis of the Porcine Reproductive and Respiratory Syndrome Virus. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/12149

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Darbellay, Joseph Andikpeme 1989-. “Elucidating the Role of Antigen-presenting Cells in the Immunopathogenesis of the Porcine Reproductive and Respiratory Syndrome Virus.” 2019. Thesis, University of Saskatchewan. Accessed March 02, 2021. http://hdl.handle.net/10388/12149.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Darbellay, Joseph Andikpeme 1989-. “Elucidating the Role of Antigen-presenting Cells in the Immunopathogenesis of the Porcine Reproductive and Respiratory Syndrome Virus.” 2019. Web. 02 Mar 2021.

Vancouver:

Darbellay JA1. Elucidating the Role of Antigen-presenting Cells in the Immunopathogenesis of the Porcine Reproductive and Respiratory Syndrome Virus. [Internet] [Thesis]. University of Saskatchewan; 2019. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/10388/12149.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Darbellay JA1. Elucidating the Role of Antigen-presenting Cells in the Immunopathogenesis of the Porcine Reproductive and Respiratory Syndrome Virus. [Thesis]. University of Saskatchewan; 2019. Available from: http://hdl.handle.net/10388/12149

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

McMaster University

26. Aljarallah, Aishah. INSIGHTS INTO THE DEVELOPMENT OF ATHEROSCLEROSIS AND CORONARY ARTERY DISEASE: STUDIES FROM GENE TARGETED MICE LACKING THE HIGH DENSITY LIPOPROTEIN RECEPTOR, SR-BI.

Degree: PhD, 2011, McMaster University

URL: http://hdl.handle.net/11375/11437

►

High density lipoprotein (HDL) is an independent risk factor for thedevelopment of coronary heart disease. HDL mediated reverse cholesterol transport is a key element… (more)

▼

High density lipoprotein (HDL) is an independent risk factor for thedevelopment of coronary heart disease. HDL mediated reverse cholesterol transport is a key element responsible for the cardioprotective effects of HDL. In addition HDL exerts other atheroprotective effects in vascular cells. The HDL receptor, scavenger receptor class I type B (SR-BI) derives the process of reverse cholesterol transport, mediates HDL signaling in the vasculature and protects against atherosclerosis. However, the exact atheroprotective mechanisms of HDL and SR-BI are not clearly understood.This thesis starts by characterizing a model of occlusive coronary arteryatherosclerosis, the SR-BI/apolipoprotein E double knockout mice and tests the effectsof phenolic rich pomegranate extract on disease progression. Coronary artery disease in these mice starts at three weeks of age and progresses rapidly leading to sudden death within three to five weeks. The administration of pomegranate extract reduced the extent of coronary artery atherosclerosis possibly via mechanisms that involved alterations in lipid metabolism and reduced inflammation and oxidative stress.The next two chapters aimed to gain better understanding of the atheroprotectiveactions of HDL and SR-BI. Increased macrophage apoptosis is a key event in the development of atherosclerotic plaques. HDL signaling via SR-BI reduced macrophage apoptosis while the lack of macrophage SR-BI was associated with increased macrophage apoptosis and necrotic core areas, features of plaque instability. Next HDL and SR-BI effects on macrophage migration, a key event in atherosclerotic plaque regression, are described. HDL stimulated the migration of macrophages in a manner that was dependent on SR-BI, its adaptor protein, PDZK1, and the G-protein coupled receptor, sphingosine-1-phosphate receptor 1. SR-BI mediated macrophage migration may suggest a potential role of SR-BI in atherosclerotic plaque regression.To expand our view of HDL effects on macrophages we have used proteomics as an approach. HDL treatment of macrophages altered the expression of multiple proteins.Validation experiment confirmed changes in interesting and particularly relevant protein targets in HDL mediated protection against macrophage apoptosis and inflammation and in HDL induced macrophage migration. Follow up experiments will determine their involvement in HDL and SR-BI mediated signaling. Overall this work represents a milestone in understanding the atheroprotective effects of HDL and SR-BI in macrophages.

Doctor of Philosophy (PhD)

Advisors/Committee Members: Trigatti, Bernardo, Geoff Werstuck and Joseph Macri, Geoff Werstuck and Joseph Macri, Biochemistry.

Subjects/Keywords: HDL; SR-BI; Macrophages; Signaling

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APA (6^th Edition):

Aljarallah, A. (2011). INSIGHTS INTO THE DEVELOPMENT OF ATHEROSCLEROSIS AND CORONARY ARTERY DISEASE: STUDIES FROM GENE TARGETED MICE LACKING THE HIGH DENSITY LIPOPROTEIN RECEPTOR, SR-BI. (Doctoral Dissertation). McMaster University. Retrieved from http://hdl.handle.net/11375/11437

Chicago Manual of Style (16^th Edition):

Aljarallah, Aishah. “INSIGHTS INTO THE DEVELOPMENT OF ATHEROSCLEROSIS AND CORONARY ARTERY DISEASE: STUDIES FROM GENE TARGETED MICE LACKING THE HIGH DENSITY LIPOPROTEIN RECEPTOR, SR-BI.” 2011. Doctoral Dissertation, McMaster University. Accessed March 02, 2021. http://hdl.handle.net/11375/11437.

MLA Handbook (7^th Edition):

Aljarallah, Aishah. “INSIGHTS INTO THE DEVELOPMENT OF ATHEROSCLEROSIS AND CORONARY ARTERY DISEASE: STUDIES FROM GENE TARGETED MICE LACKING THE HIGH DENSITY LIPOPROTEIN RECEPTOR, SR-BI.” 2011. Web. 02 Mar 2021.

Vancouver:

Aljarallah A. INSIGHTS INTO THE DEVELOPMENT OF ATHEROSCLEROSIS AND CORONARY ARTERY DISEASE: STUDIES FROM GENE TARGETED MICE LACKING THE HIGH DENSITY LIPOPROTEIN RECEPTOR, SR-BI. [Internet] [Doctoral dissertation]. McMaster University; 2011. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/11375/11437.

Council of Science Editors:

Aljarallah A. INSIGHTS INTO THE DEVELOPMENT OF ATHEROSCLEROSIS AND CORONARY ARTERY DISEASE: STUDIES FROM GENE TARGETED MICE LACKING THE HIGH DENSITY LIPOPROTEIN RECEPTOR, SR-BI. [Doctoral Dissertation]. McMaster University; 2011. Available from: http://hdl.handle.net/11375/11437

Université du Québec à Montréal

27. Warburton, Christopher. Les macrophages stimulent la production de proérythroblastes et la différentiation érythrocytaire par contact direct en absence d'EPO exogène.

Degree: 2017, Université du Québec à Montréal

URL: http://archipel.uqam.ca/9833/1/M15016.pdf

► L'érythropoïèse est principalement régulée par l'hormone rénale érythropoïétine (EPO), qui stimule la prolifération et la différentiation des précurseurs érythropoïétiques à travers des effets anti-apoptotiques et… (more)

▼ L'érythropoïèse est principalement régulée par l'hormone rénale érythropoïétine (EPO), qui stimule la prolifération et la différentiation des précurseurs érythropoïétiques à travers des effets anti-apoptotiques et antioxydants. Sous des conditions homéostatiques, les érythroblastes de la moelle osseuse s'organisent en ilots autour d'un macrophage central, qui supporte l'échange de fer nécessaire à la synthèse d'hémoglobine ainsi que la phagocytose de noyaux extrudés. Le fait que la déplétion expérimentale in vivo de macrophages cause une déficience rapide de l'érythropoïèse nous a mené à émettre l'hypothèse que les macrophages peuvent être une source d'EPO in situ, ou produisent des analogues fonctionnels à l'EPO. Afin de valider cette hypothèse, la contribution des facteurs solubles dérivés des macrophages de la moelle osseuse ainsi que l'impact d'interaction cellulaire directe ace des précurseurs hématopoïétiques ont été étudié in vitro dans des conditions de culture sans EPO. Des cellules lignées négative de la moelle osseuse, enrichies par sélection négative, ont étés mises en culture en présence de milieu conditionné par les macrophages dérivés de la moelle osseuse (BMDM), ou en contact direct avec ceux-ci, dans un milieu contenant de l'insuline humaine, de l'holotransferrine et d'albumine bovine dé-ionisée mais exempte d'EPO. L'impact de la déplétion in vivo des macrophages sur l'érythropoïèse a été étudié en injectant des liposomes de Clodronate dans des souris Balb/c. Les populations érythrocytaires ont étés analysés ex vivo par FACS en utilisant des anticorps anti-CD71 et Ter119, ou par coloration May-Grünwald et Giemsa. Nos résultats démontrent que le milieu conditionné de BMDM promeut la différentiation des stades précoces érythrocytaires (proérythroblastes) et diminue la prolifération des stades tardifs érythrocytaires. La déplétion des macrophages pendant une semaine cause un arrêt complet de l'érythropoïèse dans la moelle osseuse sans toutefois induire une production compensatoire d'EPO par le rein. L'EPO n'as pu être détectée par PCR, Western Blot ou ELISA dans les surnageant et les lysats de BMDM en condition de culture normoxique et hypoxique. Ces résultats démontrent qu'en condition expérimentale sans ajout d'EPO exogène, les macrophages de la moelle osseuse stimulent les phases précoces de différentiation érythrocytaire.

Subjects/Keywords: Érythropoïèse – Régulation; Érythropoïétine; Macrophages

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APA (6^th Edition):

Warburton, C. (2017). Les macrophages stimulent la production de proérythroblastes et la différentiation érythrocytaire par contact direct en absence d'EPO exogène. (Thesis). Université du Québec à Montréal. Retrieved from http://archipel.uqam.ca/9833/1/M15016.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Warburton, Christopher. “Les macrophages stimulent la production de proérythroblastes et la différentiation érythrocytaire par contact direct en absence d'EPO exogène.” 2017. Thesis, Université du Québec à Montréal. Accessed March 02, 2021. http://archipel.uqam.ca/9833/1/M15016.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Warburton, Christopher. “Les macrophages stimulent la production de proérythroblastes et la différentiation érythrocytaire par contact direct en absence d'EPO exogène.” 2017. Web. 02 Mar 2021.

Vancouver:

Warburton C. Les macrophages stimulent la production de proérythroblastes et la différentiation érythrocytaire par contact direct en absence d'EPO exogène. [Internet] [Thesis]. Université du Québec à Montréal; 2017. [cited 2021 Mar 02]. Available from: http://archipel.uqam.ca/9833/1/M15016.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Warburton C. Les macrophages stimulent la production de proérythroblastes et la différentiation érythrocytaire par contact direct en absence d'EPO exogène. [Thesis]. Université du Québec à Montréal; 2017. Available from: http://archipel.uqam.ca/9833/1/M15016.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto

28. Gigliozzi, Darren. Bacteria Filamentation, a Contributing Factor to the Intracellular Survival of Legionella pneumophila.

Degree: 2012, University of Toronto

URL: http://hdl.handle.net/1807/33217

►

Legionella pneumophila (Lp) is the pathogen responsible for Legionnaires disease. Lp invades and survives in human macrophages to form an intracellular compartment, called the Legionella… (more)

Subjects/Keywords: Legionella; Macrophages; 0410; 0379

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APA (6^th Edition):

Gigliozzi, D. (2012). Bacteria Filamentation, a Contributing Factor to the Intracellular Survival of Legionella pneumophila. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/33217

Chicago Manual of Style (16^th Edition):

Gigliozzi, Darren. “Bacteria Filamentation, a Contributing Factor to the Intracellular Survival of Legionella pneumophila.” 2012. Masters Thesis, University of Toronto. Accessed March 02, 2021. http://hdl.handle.net/1807/33217.

MLA Handbook (7^th Edition):

Gigliozzi, Darren. “Bacteria Filamentation, a Contributing Factor to the Intracellular Survival of Legionella pneumophila.” 2012. Web. 02 Mar 2021.

Vancouver:

Gigliozzi D. Bacteria Filamentation, a Contributing Factor to the Intracellular Survival of Legionella pneumophila. [Internet] [Masters thesis]. University of Toronto; 2012. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1807/33217.

Council of Science Editors:

Gigliozzi D. Bacteria Filamentation, a Contributing Factor to the Intracellular Survival of Legionella pneumophila. [Masters Thesis]. University of Toronto; 2012. Available from: http://hdl.handle.net/1807/33217

University of Toronto

29. Acharya, Durga. Interplay between phagocytosis and pro-inflammatory cytokine production in macrophages.

Degree: 2018, University of Toronto

URL: http://hdl.handle.net/1807/91479

►

Macrophages are able to recognize, bind and internalize pathogens through two types of phagocytic receptors; the Fc receptors (FcγR) and the complement receptors (CR). FcγRs… (more)

Subjects/Keywords: Inflammation; Macrophages; Phagocytosis; 0307

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APA (6^th Edition):

Acharya, D. (2018). Interplay between phagocytosis and pro-inflammatory cytokine production in macrophages. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/91479

Chicago Manual of Style (16^th Edition):

Acharya, Durga. “Interplay between phagocytosis and pro-inflammatory cytokine production in macrophages.” 2018. Masters Thesis, University of Toronto. Accessed March 02, 2021. http://hdl.handle.net/1807/91479.

MLA Handbook (7^th Edition):

Acharya, Durga. “Interplay between phagocytosis and pro-inflammatory cytokine production in macrophages.” 2018. Web. 02 Mar 2021.

Vancouver:

Acharya D. Interplay between phagocytosis and pro-inflammatory cytokine production in macrophages. [Internet] [Masters thesis]. University of Toronto; 2018. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1807/91479.

Council of Science Editors:

Acharya D. Interplay between phagocytosis and pro-inflammatory cytokine production in macrophages. [Masters Thesis]. University of Toronto; 2018. Available from: http://hdl.handle.net/1807/91479

Victoria University of Wellington

30. Steiger, Stefanie. The Role of TGFβ1 and Macrophage Differentiation in MSU Crystal-Induced Inflammation.

Degree: 2014, Victoria University of Wellington

URL: http://hdl.handle.net/10063/3237

► Gout is a painful form of inflammatory arthritis that is caused by the deposition of monosodium urate (MSU) crystals in the joints. MSU crystals trigger… (more)

▼ Gout is a painful form of inflammatory arthritis that is caused by the deposition of monosodium urate (MSU) crystals in the joints. MSU crystals trigger a local inflammatory response initiated by resident macrophages followed by a large infiltration of leukocytes. The spontaneous resolution of acute gout is associated with the production of transforming growth factor β1 (TGFβ1). The overall objectives of this thesis were to investigate mechanisms that lead to TGFβ1 production and contribute to the resolution of acute gout, the effect of TGFβ1 on the functional phenotype of differentiated macrophages, and possible changes in surface marker expression by macrophages in response to MSU crystals. To determine macrophage-independent sources of TGFβ1 during the resolution of acute gout and how TGFβ1 production altered MSU crystal-recruited neutrophil functions, neutrophils were purified from MSU crystal-treated mice when levels of TGFβ1 were high. MSU crystal-recruited neutrophils and circulating blood neutrophils were identified as TGFβ1⁺ cells. The mechanism for TGFβ1 production by neutrophils was associated with their ability to phagocytose apoptotic neutrophils. TGFβ1 produced by canibalising neutrophils inhibited both respiratory burst and interleukin-1β (IL-1β) production by MSU crystal-activated neutrophils ex vivo. Importantly, neutrophils from MSU crystal-challenged mice treated with TGFβ1 neutralising antibody in vivo produced elevated levels of superoxide but neutrophil IL-1β production was unaffected. These results show that TGFβ1 produced by canibalising neutrophils can actively suppress neutrophil inflammatory functions and therefore make a significant contribution towards the resolution of gouty inflammation. To investigate the effect of TGFβ1 on macrophage differentiation in vitro, granulocyte macrophage colony-stimulating factor (GM-CSF) bone marrow macrophages (GM-BMMs) and macrophage colony-stimulating factor (M-CSF) bone marrow macrophages (M-BMMs) were generated in the presence of TGFβ1. TGFβ1 was found to drive a hyper-inflammatory GM-BMM phenotype, while contributing to the differentiation of a hypo-inflammatory M-BMM phenotype specifically in response to MSU crystals. Increased IL-1β production by TGFβ1-differentiated GM-BMMs was associated with enhanced NOD like receptor family, pyrin domain-containing 3 (NLRP3) in ammasome activation and caspase 1/caspase 8 interaction, and a down-regulation of receptor-interacting serine/threonine-protein kinase 3 (RIP3) triggered by MSU crystals. At the same, TGFβ1 inhibited antigen-specific T cell proliferation by GM-BMMs. In contrast, TGFβ1-treated M-BMMs down-regulated the expression of active IL-1β that correlated with decreased IL-1β production, and upregulated RIP3 expression in response to MSU crystals. These data indicate that TGFβ1-treated GM-BMMs exhibited a hyper-inflammatory response to MSU crystal stimulation, whereas M-BMMs were found to be hypo-responsive. Macrophages were found to upregulate the surface marker NK1.1, which is primarily… Advisors/Committee Members: Harper, Jacquie, Ian, Hermans.

Subjects/Keywords: TGFβ1; Acute gouty inflammation; Macrophages

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APA (6^th Edition):

Steiger, S. (2014). The Role of TGFβ1 and Macrophage Differentiation in MSU Crystal-Induced Inflammation. (Doctoral Dissertation). Victoria University of Wellington. Retrieved from http://hdl.handle.net/10063/3237

Chicago Manual of Style (16^th Edition):

Steiger, Stefanie. “The Role of TGFβ1 and Macrophage Differentiation in MSU Crystal-Induced Inflammation.” 2014. Doctoral Dissertation, Victoria University of Wellington. Accessed March 02, 2021. http://hdl.handle.net/10063/3237.

MLA Handbook (7^th Edition):

Steiger, Stefanie. “The Role of TGFβ1 and Macrophage Differentiation in MSU Crystal-Induced Inflammation.” 2014. Web. 02 Mar 2021.

Vancouver:

Steiger S. The Role of TGFβ1 and Macrophage Differentiation in MSU Crystal-Induced Inflammation. [Internet] [Doctoral dissertation]. Victoria University of Wellington; 2014. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/10063/3237.

Council of Science Editors:

Steiger S. The Role of TGFβ1 and Macrophage Differentiation in MSU Crystal-Induced Inflammation. [Doctoral Dissertation]. Victoria University of Wellington; 2014. Available from: http://hdl.handle.net/10063/3237

Open Access Theses and Dissertations