subject:(Macrophages)

University of Hong Kong

1. Peng, Jiao. Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin.

Degree: PhD, 2015, University of Hong Kong

URL: Peng, J. [彭佼]. (2015). Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5558991 ; 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 (6^th Edition):

Peng, J. (2015). Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin. (Doctoral Dissertation). University of Hong Kong. Retrieved from Peng, J. [彭佼]. (2015). Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5558991 ; http://hdl.handle.net/10722/216268

Chicago Manual of Style (16^th Edition):

Peng, Jiao. “Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin.” 2015. Doctoral Dissertation, University of Hong Kong. Accessed February 26, 2020. Peng, J. [彭佼]. (2015). Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5558991 ; http://hdl.handle.net/10722/216268.

MLA Handbook (7^th Edition):

Peng, Jiao. “Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin.” 2015. Web. 26 Feb 2020.

Vancouver:

Peng J. Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin. [Internet] [Doctoral dissertation]. University of Hong Kong; 2015. [cited 2020 Feb 26]. Available from: Peng, J. [彭佼]. (2015). Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5558991 ; http://hdl.handle.net/10722/216268.

Council of Science Editors:

Peng J. Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin. [Doctoral Dissertation]. University of Hong Kong; 2015. Available from: Peng, J. [彭佼]. (2015). Tumor associated macrophages reprogramming : the role of TGF-beta/TLR7 and adiponectin. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5558991 ; http://hdl.handle.net/10722/216268

Penn State University

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

Degree: PhD, Anatomy, 2010, Penn State University

URL: https://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 phagocytic functional…

Subjects/Keywords: macrophages

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APA (6^th Edition):

Carroll, M. A. (2010). STAT3-Deficiency in Bone Marrow Hematopoietic Stem Cells results in Dysfunctional Macrophages and Correlates with Crohn's Disease-like Pathogenesis. (Doctoral Dissertation). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/11611

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.” 2010. Doctoral Dissertation, Penn State University. Accessed February 26, 2020. https://etda.libraries.psu.edu/catalog/11611.

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.” 2010. Web. 26 Feb 2020.

Vancouver:

Carroll MA. STAT3-Deficiency in Bone Marrow Hematopoietic Stem Cells results in Dysfunctional Macrophages and Correlates with Crohn's Disease-like Pathogenesis. [Internet] [Doctoral dissertation]. Penn State University; 2010. [cited 2020 Feb 26]. Available from: https://etda.libraries.psu.edu/catalog/11611.

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. [Doctoral Dissertation]. Penn State University; 2010. Available from: https://etda.libraries.psu.edu/catalog/11611

University of Hong Kong

3. Feng, Qian. Characterization of NG2+ macrophage in glaucoma : an investigation focusing on its origin and potential roles in ischemic retina.

Degree: PhD, 2014, University of Hong Kong

URL: Feng, Q. [馮茜]. (2014). Characterization of NG2+ macrophage in glaucoma : an investigation focusing on its origin and potential roles in ischemic retina. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5185941 ; http://dx.doi.org/10.5353/th_b5185941 ; http://hdl.handle.net/10722/197102

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Macrophage manipulation as immunomodulatory intervention in glaucoma, a leading cause to blindness characterized by retinal ganglion cell (RGC) loss, has been proposed as a promising… (more)

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Macrophage manipulation as immunomodulatory intervention in glaucoma, a leading cause to blindness characterized by retinal ganglion cell (RGC) loss, has been proposed as a promising strategy to protect RGCs from dying. Three types of macrophage in damaged retinas, microglia-derived macrophage, monocyte-derived macrophage and perivascular macrophage, together consist a highly heterogeneous population with both beneficial and detrimental functions partly resulted from their distinct origins. NG2 (Nerve/glial antigen 2) positive macrophage, a subtype of macrophage, has been considered to fulfill specific functions with neuroprotective and neurogenic potentials. Whether NG2+ macrophage can be a possible target for treatment in glaucoma is unknown. Basic information of this subtype of macrophage in ischemic retinas of a mouse glaucomatous model called acute ocular hypertension (AOH) model was obtained in this study to answer three questions. First, do NG2+ macrophage exist in mouse retina, if so, what do they like? In normal mouse retinas, NG2+ macrophage did not exist. After AOH, NG2 could be induced on macrophage. And they are unevenly distributed in the whole retina while reside in the ganglion cell layer, inner plexiform layer or inner nuclear layer. Moreover, NG2+ macrophage all contained two nuclei with typical amoeboid-like morphologies of macrophage in activation state except the rounded type. Secondly, are they associated with the surrounding cells, if so, how? Close association of RGCs and Müller cells with NG2+ macrophage was found due to their co-localization. To know how they functioned, potential roles regarding its proliferating and phagocytic abilities were revealed by its co-localization with proliferating and phagocytic markers. However, unlike NG2+ macrophage in ischemic brain, NG2+ macrophage in ischemic retina did not express neurotrophic factors while some of them were found to express interlukin-10, an anti-inflammatory cytokine. Possible neurogenic potential was also observed by its co-localization with Nestin, a neural stem cell marker. Thirdly, where do they come from? To know their origins, bone marrow chimeras combined with specific markers were used to distinguish microglia-derived macrophage, monocyte-derived macrophage and perivascular macrophage. And it was found that majority of NG2+ macrophage was originated from resident microglia, rather than monocyte-derived macrophage or perivascular macrophage. Taken together, the present study showed the basic profile of a subtype of macrophage in a mouse model of glaucoma, more accurately, NG2+ macrophage in AOH mouse retinas. NG2 expression was induced mostly in resident microglia in AOH retina as a proliferating population with phagocytic, anti-inflammatory functions, and possible neurogenic potentials. Therefore, NG2+ macrophage may be a potential candidate target for treatment of glaucoma.

published_or_final_version

Anatomy

Doctoral

Doctor of Philosophy

Advisors/Committee Members: So, KF, Chung, SK.

Subjects/Keywords: Glaucoma; Macrophages

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APA (6^th Edition):

Feng, Q. (2014). Characterization of NG2+ macrophage in glaucoma : an investigation focusing on its origin and potential roles in ischemic retina. (Doctoral Dissertation). University of Hong Kong. Retrieved from Feng, Q. [馮茜]. (2014). Characterization of NG2+ macrophage in glaucoma : an investigation focusing on its origin and potential roles in ischemic retina. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5185941 ; http://dx.doi.org/10.5353/th_b5185941 ; http://hdl.handle.net/10722/197102

Chicago Manual of Style (16^th Edition):

Feng, Qian. “Characterization of NG2+ macrophage in glaucoma : an investigation focusing on its origin and potential roles in ischemic retina.” 2014. Doctoral Dissertation, University of Hong Kong. Accessed February 26, 2020. Feng, Q. [馮茜]. (2014). Characterization of NG2+ macrophage in glaucoma : an investigation focusing on its origin and potential roles in ischemic retina. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5185941 ; http://dx.doi.org/10.5353/th_b5185941 ; http://hdl.handle.net/10722/197102.

MLA Handbook (7^th Edition):

Feng, Qian. “Characterization of NG2+ macrophage in glaucoma : an investigation focusing on its origin and potential roles in ischemic retina.” 2014. Web. 26 Feb 2020.

Vancouver:

Feng Q. Characterization of NG2+ macrophage in glaucoma : an investigation focusing on its origin and potential roles in ischemic retina. [Internet] [Doctoral dissertation]. University of Hong Kong; 2014. [cited 2020 Feb 26]. Available from: Feng, Q. [馮茜]. (2014). Characterization of NG2+ macrophage in glaucoma : an investigation focusing on its origin and potential roles in ischemic retina. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5185941 ; http://dx.doi.org/10.5353/th_b5185941 ; http://hdl.handle.net/10722/197102.

Council of Science Editors:

Feng Q. Characterization of NG2+ macrophage in glaucoma : an investigation focusing on its origin and potential roles in ischemic retina. [Doctoral Dissertation]. University of Hong Kong; 2014. Available from: Feng, Q. [馮茜]. (2014). Characterization of NG2+ macrophage in glaucoma : an investigation focusing on its origin and potential roles in ischemic retina. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5185941 ; http://dx.doi.org/10.5353/th_b5185941 ; http://hdl.handle.net/10722/197102

University of Aberdeen

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

Degree: 2012, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=185639 ; http://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 · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kluge, C. (2012). Regulating human Th17 polarisation by activated macrophages. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=185639 ; http://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 February 26, 2020. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=185639 ; http://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. 26 Feb 2020.

Vancouver:

Kluge C. Regulating human Th17 polarisation by activated macrophages. [Internet] [Doctoral dissertation]. University of Aberdeen; 2012. [cited 2020 Feb 26]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=185639 ; http://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: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=185639 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.553806

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 February 26, 2020. 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. 26 Feb 2020.

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 2020 Feb 26]. 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, 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://digitool2.abdn.ac.uk:1801/webclient/DeliveryManager?pid=185639&custom_att_2=simple_viewer

Subjects/Keywords: Macrophages

Record Details Similar Records Cite « Share

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

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://digitool2.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 February 26, 2020. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=185639 ; http://digitool2.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. 26 Feb 2020.

Vancouver:

Kluge, Christina E. Regulating human Th17 polarisation by activated macrophages. [Internet] [Doctoral dissertation]. University of Aberdeen; 2012. [cited 2020 Feb 26]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=185639 ; http://digitool2.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://digitool2.abdn.ac.uk:1801/webclient/DeliveryManager?pid=185639&custom_att_2=simple_viewer

University of Arizona

7. 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 February 26, 2020. 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. 26 Feb 2020.

Vancouver:

Elvick, Allen LeRoy 1. Enzyme profiles of control and sulfuric acid aerosol stressed alveolar macrophages . [Internet] [Masters thesis]. University of Arizona; 1978. [cited 2020 Feb 26]. 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

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

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 February 26, 2020. 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. 26 Feb 2020.

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 2020 Feb 26]. 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

University of Rochester

9. VanWinkle, Beth Ann; Gunter, Thomas E. Monocytes and Their Mitochondria in Alzheimer's Disease.

Degree: PhD, 2010, University of Rochester

URL: http://hdl.handle.net/1802/10502

► Mitochondrial ultra structure appears abnormal in human neurons in end stage Alzheimer’s disease (AD). Alterations in cristae structure and fragmented mitochondria have been reported. We… (more)

▼ Mitochondrial ultra structure appears abnormal in human neurons in end stage Alzheimer’s disease (AD). Alterations in cristae structure and fragmented mitochondria have been reported. We observe a similar loss of mitochondrial cristae structure in a blood cell model induced by diazoxide (Dz), a known K-ATP channel activator. In the blood cell model, Dz altered mitochondrial structure and also protected the cells from a potent inducer of apoptosis. The apoptotic protection of Dz extended to a neuronal cell model in their un-differentiated state with no Dz protection afforded after the neuronal cells differentiated. Whether or not Dz altered mitochondrial structure in the neuronal model was not determined. The dual effects of Dz, on mitochondrial structure and on apoptotic protection, appear to occur on different time-scales and it was not clear if the Dz effect on mitochondrial structure was related to Dz apoptotic protection. Primary blood cells were examined to investigate both effects of Dz. Monocytes could be protected from apoptosis with Dz pre-treatment and monocyte mitochondrial structure was altered in a dose dependent manner within the Dz one-hour pre-treatment period. The Dz dose required to confer apoptotic protection produced slight alterations in mitochondrial structure but a higher dose produced mitochondrial structure like mitochondrial structure previously reported in neurons of AD patients. Since mitochondrial structure in primary blood cells could be induced to appear identical to mitochondria in AD neurons and blood cells are affected in AD, our goal became to determine if morphological variation would be evident in AD blood cells and/or their mitochondria. The hypothesis that structural anomalies exist in tissue outside the brain in AD was tested by close examination of blood cells, specifically monocytes, from human donors. Whole blood was donated and peripheral blood mononuclear cells (PBMCs) were isolated. An aliquot of PBMCs was fixed immediately for transmission electron microscopy (TEM) and then viewed to identify and count monocytes. ImageJ, image analysis software, was used for all measurements in TEM pictures including the number of native monocytes per grid space, the primary monocyte size, and the mitochondrial number/size/circularity per cell. Macrophages were selected from the remaining PBMCs by plating and in vitro differentiated for seven days. These monocyte-derived macrophages (MDMs) were counted for each donor sample. All samples were collected and analyzed blind, without any specific knowledge of the donors. After case identification, the AD data was compared to aged control (no-clinical sign of AD) or “NC” data. The AD donors display a two-fold increase in native monocytes over NC donors. The AD native monocytes were on average 70% larger with 50% more individual mitochondria per cell than those isolated from NC donors. The AD monocyte mitochondria were smaller and more circular in the majority of the AD cells, indicative of fragmented…

Subjects/Keywords: Mitochondria; Alzheimer's; Monocytes; Macrophages; Monocyte Derived Macrophages

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APA (6^th Edition):

VanWinkle, Beth Ann; Gunter, T. E. (2010). Monocytes and Their Mitochondria in Alzheimer's Disease. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/10502

Chicago Manual of Style (16^th Edition):

VanWinkle, Beth Ann; Gunter, Thomas E. “Monocytes and Their Mitochondria in Alzheimer's Disease.” 2010. Doctoral Dissertation, University of Rochester. Accessed February 26, 2020. http://hdl.handle.net/1802/10502.

MLA Handbook (7^th Edition):

VanWinkle, Beth Ann; Gunter, Thomas E. “Monocytes and Their Mitochondria in Alzheimer's Disease.” 2010. Web. 26 Feb 2020.

Vancouver:

VanWinkle, Beth Ann; Gunter TE. Monocytes and Their Mitochondria in Alzheimer's Disease. [Internet] [Doctoral dissertation]. University of Rochester; 2010. [cited 2020 Feb 26]. Available from: http://hdl.handle.net/1802/10502.

Council of Science Editors:

VanWinkle, Beth Ann; Gunter TE. Monocytes and Their Mitochondria in Alzheimer's Disease. [Doctoral Dissertation]. University of Rochester; 2010. Available from: http://hdl.handle.net/1802/10502

10. 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 February 26, 2020. 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. 26 Feb 2020.

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 2020 Feb 26]. 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

11. 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 February 26, 2020. 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. 26 Feb 2020.

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 2020 Feb 26]. 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

University of Aberdeen

12. Liu, Yu. The role of suppressors of cytokine signalling 1 and 3 in macrophage activation.

Degree: 2008, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=24848 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493453

► Macrophages (M?) are widely distributed immune cells and can be phenotypically polarised by microenvironment to mount specific functional programs. M? polarised in vitro can be… (more)

Subjects/Keywords: 616.07995; Macrophages : Cytokines

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APA (6^th Edition):

Liu, Y. (2008). The role of suppressors of cytokine signalling 1 and 3 in macrophage activation. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=24848 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493453

Chicago Manual of Style (16^th Edition):

Liu, Yu. “The role of suppressors of cytokine signalling 1 and 3 in macrophage activation.” 2008. Doctoral Dissertation, University of Aberdeen. Accessed February 26, 2020. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=24848 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493453.

MLA Handbook (7^th Edition):

Liu, Yu. “The role of suppressors of cytokine signalling 1 and 3 in macrophage activation.” 2008. Web. 26 Feb 2020.

Vancouver:

Liu Y. The role of suppressors of cytokine signalling 1 and 3 in macrophage activation. [Internet] [Doctoral dissertation]. University of Aberdeen; 2008. [cited 2020 Feb 26]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=24848 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493453.

Council of Science Editors:

Liu Y. The role of suppressors of cytokine signalling 1 and 3 in macrophage activation. [Doctoral Dissertation]. University of Aberdeen; 2008. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=24848 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493453

Texas A&M University

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

Degree: 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 (6^th Edition):

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

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):

Kanameni, Srikanth. “Transcriptional Profiling of Polarized Macrophages using RNA-Sequencing.” 2015. Thesis, Texas A&M University. Accessed February 26, 2020. http://hdl.handle.net/1969.1/155022.

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

MLA Handbook (7^th Edition):

Kanameni, Srikanth. “Transcriptional Profiling of Polarized Macrophages using RNA-Sequencing.” 2015. Web. 26 Feb 2020.

Vancouver:

Kanameni S. Transcriptional Profiling of Polarized Macrophages using RNA-Sequencing. [Internet] [Thesis]. Texas A&M University; 2015. [cited 2020 Feb 26]. Available from: http://hdl.handle.net/1969.1/155022.

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

Council of Science Editors:

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

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

University of Hong Kong

14. 林薏芙.; Lam, Yi-Fu, Eve. The biological activities of glycodelin-A on human monocytes and macrophages.

Degree: M. Phil., 2011, University of Hong Kong

URL: Lam, Y. F. E. [林薏芙]. (2011). The biological activities of glycodelin-A on human monocytes and macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775254 ; http://dx.doi.org/10.5353/th_b4775254 ; http://hdl.handle.net/10722/180815

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The fetal-maternal interface is an immunologically privileged site where the semi-allogeneic fetus is protected from the maternal immune system. Macrophage represents the second major type… (more)

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The fetal-maternal interface is an immunologically privileged site where the semi-allogeneic fetus is protected from the maternal immune system. Macrophage represents the second major type (20-30%) of the decidual leukocyte. It functions as important regulator of pregnancy processes such as fetal tolerance, placental development and onset of labor. Changes in macrophage number and activity have been associated with fetal loss and pregnancy complications, including intrauterine growth restriction and preeclampsia. Glycodelin-A (Gd-A) is an abundant glycoprotein with ubiquitous distribution in the first trimester deciduas. It is suggested to be involved in early placental development by its regulatory activities on various immune cells. In this study, it is hypothesized that Gd-A has regulatory role in monocyte/macrophage functions and differentiation. The first objective examined the role of Gd-A in the biological activities of monocytes and macrophages. Gd-A was found to bind to the monocytic cell lines THP-1 and U937, blood monocytes, granulocyte macrophage colony-stimulating factor (GM-CSF)-differentiated macrophages, phorbol 12-myristate 13-acetate-differentiated macrophage and blood macrophages. Gd-A did not affect the viability, proliferation, cell death and phagocytic activity of monocytes and macrophages. The second objective examined the effect of Gd-A on the cytokine secretion of monocytes and macrophages. Gd-A treatment increased the IL-6 production in monocytes and macrophages. IL-6 was associated with the development and growth of the fetal-placental unit. Gd-A also induced the extracellular signal regulated kinases (ERK) activation. The involvement of ERK in stimulating IL-6 production was confirmed by using pharmacological inhibitors. Monocytes in the blood stream are attracted and residue into the deciduas, which differentiated into macrophage under the influence of various decidual soluble factors. Therefore, the third objective studied the possible involvement of Gd-A on the differentiation of monocytes into macrophages. Co-treatment of Gd-A during the GM-CSF-induced differentiation of monocytes stimulated the indoleamine 2,3-dioxygenase (IDO-1) expression and activity in differentiated macrophages. These differentiated macrophages inhibited the proliferation of autologous peripheral blood mononuclear cell in the co-culture system by G0/G1 cell cycle arrest. IDO-1 is one of the reported decidual macrophage markers. It has been suggested to be involved in establishing the tolerogenic environment during pregnancy through L-tryptophan depletion. The increase in IDO-1 expression may be regulated by PKC signaling pathway. Taken together, this thesis reported a novel role of Gd-A on the monocyte differentiation. The present results enhance our knowledge on the regulation of early placentation in human and may shed light on understanding the pathology of complicated pregnancy due to macrophage dysfunction.

published_or_final_version

Obstetrics and Gynaecology

Master

Master of Philosophy

Subjects/Keywords: Glycoproteins.; Monocytes.; Macrophages.

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APA (6^th Edition):

林薏芙.; Lam, Yi-Fu, E. (2011). The biological activities of glycodelin-A on human monocytes and macrophages. (Masters Thesis). University of Hong Kong. Retrieved from Lam, Y. F. E. [林薏芙]. (2011). The biological activities of glycodelin-A on human monocytes and macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775254 ; http://dx.doi.org/10.5353/th_b4775254 ; http://hdl.handle.net/10722/180815

Chicago Manual of Style (16^th Edition):

林薏芙.; Lam, Yi-Fu, Eve. “The biological activities of glycodelin-A on human monocytes and macrophages.” 2011. Masters Thesis, University of Hong Kong. Accessed February 26, 2020. Lam, Y. F. E. [林薏芙]. (2011). The biological activities of glycodelin-A on human monocytes and macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775254 ; http://dx.doi.org/10.5353/th_b4775254 ; http://hdl.handle.net/10722/180815.

MLA Handbook (7^th Edition):

林薏芙.; Lam, Yi-Fu, Eve. “The biological activities of glycodelin-A on human monocytes and macrophages.” 2011. Web. 26 Feb 2020.

Vancouver:

林薏芙.; Lam, Yi-Fu E. The biological activities of glycodelin-A on human monocytes and macrophages. [Internet] [Masters thesis]. University of Hong Kong; 2011. [cited 2020 Feb 26]. Available from: Lam, Y. F. E. [林薏芙]. (2011). The biological activities of glycodelin-A on human monocytes and macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775254 ; http://dx.doi.org/10.5353/th_b4775254 ; http://hdl.handle.net/10722/180815.

Council of Science Editors:

林薏芙.; Lam, Yi-Fu E. The biological activities of glycodelin-A on human monocytes and macrophages. [Masters Thesis]. University of Hong Kong; 2011. Available from: Lam, Y. F. E. [林薏芙]. (2011). The biological activities of glycodelin-A on human monocytes and macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775254 ; http://dx.doi.org/10.5353/th_b4775254 ; http://hdl.handle.net/10722/180815

University of Hong Kong

15. 李及彬; Li, Jibin. Mechanisms underlying differential infection by pandemic H1N1 influenza A virus of human classically activated and alternativelyactivated macrophages.

Degree: M. Phil., 2012, University of Hong Kong

URL: Li, J. [李及彬]. (2012). Mechanisms underlying differential infection by pandemic H1N1 influenza A virus of human classically activated and alternatively activated macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4961754 ; http://dx.doi.org/10.5353/th_b4961754 ; http://hdl.handle.net/10722/180934

► Macrophages have well-established roles in the primary response to pathogens and hold essential functions during innate and adaptive immunity. Under activation by different growth factors… (more)

▼ Macrophages have well-established roles in the primary response to pathogens and hold essential functions during innate and adaptive immunity. Under activation by different growth factors and cytokines, human monocytes have been shown to differentiate and polarize into two main types of macrophage, classically-activated macrophages (caMφ) and alternatively-activated macrophages (aaMφ), displaying distinct properties and phenotypes. For instance, caMφ secrete pro-inflammatory cytokines, whereas aaM secrete anti-inflammatory cytokines. Additionally, aaMφ displays stronger phagocytic ability and are equipped with different endosomal proteases. While it has been established that monocyte-derived macrophages can be infected by Influenza A virus, most studies utilized a macrophage population obtained by differentiation in the presence of autologous plasma. My research project aimed at systematically comparing susceptibility of the infection by Influenza A virus to the recently described caMφ and aaMφ. Here I show that monocytes cultured in presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) and interferon (IFN)-γ or in presence of macrophage colony-stimulating factor (M-CSF) and interleukin (IL)-4 or IL-10 can be differentiated into distinct populations. According to immunophenotyping results, a distinct expression profile was observed for Cluster of Differentiation (CD) 36, CD86, Mannose Receptor (MR or CD206), and Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrin (DC-SIGN or CD209) among differentiated macrophages. Except for CD86 expression, my results were in accordance with previous reports and thus allowed me to classify all populations into caMφ (M1 macrophages), and aaMφ (M2a and M2c macrophages). I then assessed the susceptibility of the above mentioned macrophages to pandemic Influenza A/California/04/2009 H1N1 virus (CA04) infection. My results demonstrate a marked difference, caMφ showing low to moderate permissivity, whereas aaMφ – and in particular M2a macrophages – were consistently highly infected. In contrast, no difference was observed with Influenza A/WSN/1933 H1N1 virus (WSN/33) infection. Because sialic acids are regarded as the primary receptor for influenza virus, I investigated the cell surface distribution of sialic acids with α2-3 linkage (SAα-2,3) or α2-6 linkage (SAα-2,6) among the population of human macrophages. By using lectin staining with Maackia amurensis lectin (MAL) II and Sambucus nigra lectin (SNA), which bind sialic acids with α2-3 linkage (SAα-2,3) and α2-6 linkage (SAα-2,6) respectively, I found all the monocyte-derived macrophages exhibited a comparable expression of SAα-2,3 and SAα-2,6, which unlikely explain the differential susceptibility to infection by CA04. In addition to sialic acids, C-type lectins were also proposed to mediate entry of influenza viruses into macrophages. All macrophages expressed CD206 but only M2a expressed CD209. However assay aiming at interfering with CD209 binding (MAb blocking assay or EGTA treatment)… Advisors/Committee Members: Lu, L, Bruzzone, R.

Subjects/Keywords: H1N1 influenza.; Macrophages.

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APA (6^th Edition):

李及彬; Li, J. (2012). Mechanisms underlying differential infection by pandemic H1N1 influenza A virus of human classically activated and alternativelyactivated macrophages. (Masters Thesis). University of Hong Kong. Retrieved from Li, J. [李及彬]. (2012). Mechanisms underlying differential infection by pandemic H1N1 influenza A virus of human classically activated and alternatively activated macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4961754 ; http://dx.doi.org/10.5353/th_b4961754 ; http://hdl.handle.net/10722/180934

Chicago Manual of Style (16^th Edition):

李及彬; Li, Jibin. “Mechanisms underlying differential infection by pandemic H1N1 influenza A virus of human classically activated and alternativelyactivated macrophages.” 2012. Masters Thesis, University of Hong Kong. Accessed February 26, 2020. Li, J. [李及彬]. (2012). Mechanisms underlying differential infection by pandemic H1N1 influenza A virus of human classically activated and alternatively activated macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4961754 ; http://dx.doi.org/10.5353/th_b4961754 ; http://hdl.handle.net/10722/180934.

MLA Handbook (7^th Edition):

李及彬; Li, Jibin. “Mechanisms underlying differential infection by pandemic H1N1 influenza A virus of human classically activated and alternativelyactivated macrophages.” 2012. Web. 26 Feb 2020.

Vancouver:

李及彬; Li J. Mechanisms underlying differential infection by pandemic H1N1 influenza A virus of human classically activated and alternativelyactivated macrophages. [Internet] [Masters thesis]. University of Hong Kong; 2012. [cited 2020 Feb 26]. Available from: Li, J. [李及彬]. (2012). Mechanisms underlying differential infection by pandemic H1N1 influenza A virus of human classically activated and alternatively activated macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4961754 ; http://dx.doi.org/10.5353/th_b4961754 ; http://hdl.handle.net/10722/180934.

Council of Science Editors:

李及彬; Li J. Mechanisms underlying differential infection by pandemic H1N1 influenza A virus of human classically activated and alternativelyactivated macrophages. [Masters Thesis]. University of Hong Kong; 2012. Available from: Li, J. [李及彬]. (2012). Mechanisms underlying differential infection by pandemic H1N1 influenza A virus of human classically activated and alternatively activated macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4961754 ; http://dx.doi.org/10.5353/th_b4961754 ; http://hdl.handle.net/10722/180934

University of Hong Kong

16. Yeung, Wai-ho. Alternatively activated macrophages promoted tumor growth and metastasis in hepatocellular carcinoma.

Degree: PhD, 2013, University of Hong Kong

URL: Yeung, W. [楊偉豪]. (2013). Alternatively activated macrophages promoted tumor growth and metastasis in hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5053410 ; http://dx.doi.org/10.5353/th_b5053410 ; http://hdl.handle.net/10722/188291

► Background and Aim Hepatocellular Carcinoma (HCC) is the fifth most frequent malignancy worldwide with high mortality and recurrence rate. Chronic inflammation is a dominant risk… (more)

▼ Background and Aim Hepatocellular Carcinoma (HCC) is the fifth most frequent malignancy worldwide with high mortality and recurrence rate. Chronic inflammation is a dominant risk factor for the malignancy and the roles of tumor associated immunological infiltrates during the disease development and progression remain unclear. The significance of alternative activated macrophages (M2) with pro-tumor phenotypes has been demonstrated in many cancers except HCC. M2 macrophages are associated with tumor angiogenesis, invasion and growth which represent a potential target to be investigated. In this study, we intend to investigate the role of M2 macrophage on HCC. Materials and Methods M2 macrophages in 100 clinical specimens collected from HCC patients were detected by immunohistochemical (IHC) staining and quantitative PCR using common macrophage markers CD14 and CD68, and M2 specific markers CD163, Scavenger receptor class A (SA) and Mannose receptor (MR). The protein and transcript expression levels were further correlated with clinical pathological parameters. Phenotypic and functional characteristics of M1 and M2 macrophages derived from THP-1 cell line were validated and their roles in promoting HCC growth and invasion were studied in vitro co-culture system and in vivo orthotopic mice model. Secretory profiles of M2 macrophages after cocultivated with HCC cells were analyzed by cytokines antibody array screening. C-C motif chemokine 22 (CCL22) was identified to be upregulated in M2 macrophages in response to HCC cells. The functional roles of the chemokine in HCC was further studied by chemotaxis and migration assay. Underlying molecular mechanisms induced by CCL22 in HCC cells were determined. Results In clinical analysis, we first discovered that macrophages were widely expressed in liver tumor comprising 10-30% of total cell population. Noteworthy, the density of a M2 macrophage marker CD163 was found to had a significant prognostic impact as an independent factor associated disease free survival (HR: 3.79; 95% CI 1.3-10.4; p<0.01). Strong expression of the CD163+ population was also correlated with poor relapse free survival, multiple tumor nodules and increased venous infiltration. In vivo studies revealed that the tumor volume injected with M2 macrophages increased 3.26-fold (1.27cm3±0.36) compared to the control group (0.39cm3±0.05) (P=0.032). In contrast, mice injected with M1 macrophages had a significant reduction of tumor volume by 2.79-fold (0.14cm3±0.02) (P=0.044). Increasing rate of lung metastases (57%) was also observed in M2 treated group compared to the control (25%) (P<0.05). In vitro, M2 macrophages increased the number of HCC cells (MHCC97L) and migration events by 1.3-fold and 3.2-fold after cocultivation compared to negative control (P<0.05). In cytokine antibody array study, M2 macrophages derived CCL22 was discovered to be strongly induced by MHCC97L. Chemotaxis analysis confirmed that CCL22 increased MHCC97L migration capacities and excess level led to increased venous… Advisors/Committee Members: Guan, X, Poon, RTP, Man, K.

Subjects/Keywords: Macrophages.; Liver - Cancer.

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APA (6^th Edition):

Yeung, W. (2013). Alternatively activated macrophages promoted tumor growth and metastasis in hepatocellular carcinoma. (Doctoral Dissertation). University of Hong Kong. Retrieved from Yeung, W. [楊偉豪]. (2013). Alternatively activated macrophages promoted tumor growth and metastasis in hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5053410 ; http://dx.doi.org/10.5353/th_b5053410 ; http://hdl.handle.net/10722/188291

Chicago Manual of Style (16^th Edition):

Yeung, Wai-ho. “Alternatively activated macrophages promoted tumor growth and metastasis in hepatocellular carcinoma.” 2013. Doctoral Dissertation, University of Hong Kong. Accessed February 26, 2020. Yeung, W. [楊偉豪]. (2013). Alternatively activated macrophages promoted tumor growth and metastasis in hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5053410 ; http://dx.doi.org/10.5353/th_b5053410 ; http://hdl.handle.net/10722/188291.

MLA Handbook (7^th Edition):

Yeung, Wai-ho. “Alternatively activated macrophages promoted tumor growth and metastasis in hepatocellular carcinoma.” 2013. Web. 26 Feb 2020.

Vancouver:

Yeung W. Alternatively activated macrophages promoted tumor growth and metastasis in hepatocellular carcinoma. [Internet] [Doctoral dissertation]. University of Hong Kong; 2013. [cited 2020 Feb 26]. Available from: Yeung, W. [楊偉豪]. (2013). Alternatively activated macrophages promoted tumor growth and metastasis in hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5053410 ; http://dx.doi.org/10.5353/th_b5053410 ; http://hdl.handle.net/10722/188291.

Council of Science Editors:

Yeung W. Alternatively activated macrophages promoted tumor growth and metastasis in hepatocellular carcinoma. [Doctoral Dissertation]. University of Hong Kong; 2013. Available from: Yeung, W. [楊偉豪]. (2013). Alternatively activated macrophages promoted tumor growth and metastasis in hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5053410 ; http://dx.doi.org/10.5353/th_b5053410 ; http://hdl.handle.net/10722/188291

University of Southern California

17. 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/5205

► 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 (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/5205

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 February 26, 2020. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/354987/rec/5205.

MLA Handbook (7^th Edition):

Margol, Ashley S. “Presence of tumor associated macrophages in SHH medulloblastoma.” 2014. Web. 26 Feb 2020.

Vancouver:

Margol AS. Presence of tumor associated macrophages in SHH medulloblastoma. [Internet] [Masters thesis]. University of Southern California; 2014. [cited 2020 Feb 26]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/354987/rec/5205.

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/5205

University of Manitoba

18. 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 (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 February 26, 2020. http://hdl.handle.net/1993/31616.

MLA Handbook (7^th Edition):

Mohammed, Ashfaque. “SEMA3E REGULATES RESIDENT MACROPHAGES RESPONSE IN LIPOPOLYSACCHARIDE-INDUCED SEPSIS.” 2016. Web. 26 Feb 2020.

Vancouver:

Mohammed A. SEMA3E REGULATES RESIDENT MACROPHAGES RESPONSE IN LIPOPOLYSACCHARIDE-INDUCED SEPSIS. [Internet] [Masters thesis]. University of Manitoba; 2016. [cited 2020 Feb 26]. 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

Rutgers University

19. 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 (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 February 26, 2020. 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. 26 Feb 2020.

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 2020 Feb 26]. 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/

University of Alberta

20. 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 February 26, 2020. 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. 26 Feb 2020.

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 2020 Feb 26]. 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

Texas A&M University

21. Allen, Charlotte Annette. Cytokine detection in eiav-infected equine monocyte-derived macrophages using quantitative real-time polymerase chain reaction.

Degree: 2009, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-2124

► The replication of equine infectious anemia virus (EIAV) in macrophages not only leads to cell death, but also to the induction of a variety of… (more)

Subjects/Keywords: Cytokines; Macrophages; Horse; QPCR

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APA (6^th Edition):

Allen, C. A. (2009). Cytokine detection in eiav-infected equine monocyte-derived macrophages using quantitative real-time polymerase chain reaction. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2124

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):

Allen, Charlotte Annette. “Cytokine detection in eiav-infected equine monocyte-derived macrophages using quantitative real-time polymerase chain reaction.” 2009. Thesis, Texas A&M University. Accessed February 26, 2020. http://hdl.handle.net/1969.1/ETD-TAMU-2124.

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

MLA Handbook (7^th Edition):

Allen, Charlotte Annette. “Cytokine detection in eiav-infected equine monocyte-derived macrophages using quantitative real-time polymerase chain reaction.” 2009. Web. 26 Feb 2020.

Vancouver:

Allen CA. Cytokine detection in eiav-infected equine monocyte-derived macrophages using quantitative real-time polymerase chain reaction. [Internet] [Thesis]. Texas A&M University; 2009. [cited 2020 Feb 26]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2124.

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

Council of Science Editors:

Allen CA. Cytokine detection in eiav-infected equine monocyte-derived macrophages using quantitative real-time polymerase chain reaction. [Thesis]. Texas A&M University; 2009. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2124

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

University of Aberdeen

22. Okai, Blessing. The role of Rab14 in the maturation of macrophage phagosomes containing Candida albicans.

Degree: PhD, 2014, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=214847 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.629398

► The virulence of the opportunistic fungal pathogen Candida albicans is in part due to its ability to switch between a yeast and hyphal form; permitting… (more)

▼ The virulence of the opportunistic fungal pathogen Candida albicans is in part due to its ability to switch between a yeast and hyphal form; permitting physical rupture and escape from macrophages after phagocytosis. This interesting feature makes C. albicans a good model organism to study in the context of phagosome maturation and in particular, the role of the small GTPase Rab14 in this process. Rab14 is recruited to bacterial phagosomes containing Chlamydia trachomatis (Capmany & Damiani, 2010) and Mycobacterium bovis BCG (Kyei et al, 2006) and aids their survival in macrophages but its role in phagosomes containing fungal pathogens is not known. Here, an important role for Rab14 in protecting macrophages against hyphal mediated lysis by C. albicans is demonstrated. Macrophages were transfected to express eGFP-Rab14, or dominant negative variants (eGFP-Rab14 S25N and eGFP-Rab14N124I); or were transfected with anti-Rab14 siRNA; then infected with live C. albicans and observed using sophisticated live cell imaging and analysis tools. Phagosomes containing live C. albicans became transiently Rab14-positive within 2 minutes following engulfment. Interestingly, a prolonged retention of Rab14 on phagosomes depended on C. albicans morphology. Phagosomes containing hyphal forms retained Rab14 for twice as long as for phagosomes containing the yeast form. Depletion of endogenous Rab14 did not affect macrophage migration towards C. albicans, the rate of engulfment or acquisition of markers of early phagosome maturation to phagosomes containing C. albicans. Furthermore, reduced Rab14 expression did not influence the kinetics of Rab5 localisation to phagosomes in macrophages that were co-transfected. Importantly, partially depleting Rab14 delayed the appearance of late phagosome maturation indicators LAMP1 and activated cathepsin in phagosomes containing live C. albicans.Rab14 knockdown was associated with a significant increase in macrophage killing by C. alibica The data presented in this thesis demonstrate the dynamic relationship between host and pathogen which can be visualised in real time at the level of individual phagosomes. Rab14 plays an important role during phagosome maturation which impacts on the later stages of phagosome maturation and is important for phagocyte survival after phagocytosis of C. albicans.

Subjects/Keywords: 610; Candida albicans; Macrophages; Phagosomes

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APA (6^th Edition):

Okai, B. (2014). The role of Rab14 in the maturation of macrophage phagosomes containing Candida albicans. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=214847 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.629398

Chicago Manual of Style (16^th Edition):

Okai, Blessing. “The role of Rab14 in the maturation of macrophage phagosomes containing Candida albicans.” 2014. Doctoral Dissertation, University of Aberdeen. Accessed February 26, 2020. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=214847 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.629398.

MLA Handbook (7^th Edition):

Okai, Blessing. “The role of Rab14 in the maturation of macrophage phagosomes containing Candida albicans.” 2014. Web. 26 Feb 2020.

Vancouver:

Okai B. The role of Rab14 in the maturation of macrophage phagosomes containing Candida albicans. [Internet] [Doctoral dissertation]. University of Aberdeen; 2014. [cited 2020 Feb 26]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=214847 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.629398.

Council of Science Editors:

Okai B. The role of Rab14 in the maturation of macrophage phagosomes containing Candida albicans. [Doctoral Dissertation]. University of Aberdeen; 2014. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=214847 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.629398

University of Edinburgh

23. Michlewska, Sylwia. Macrophage phagocytosis of apoptotic neutrophils is critically regulated by the opposing actions of pro-inflammatory and anti-inflammatory agents : key role for TNF-α.

Degree: PhD, 2011, University of Edinburgh

URL: http://hdl.handle.net/1842/5594

► Development of chronic inflammation or autoimmunity may be related to deregulated mechanisms orchestrating successful resolution of inflammation, especially apoptosis of inflammatory cells and their subsequent… (more)

▼ Development of chronic inflammation or autoimmunity may be related to deregulated mechanisms orchestrating successful resolution of inflammation, especially apoptosis of inflammatory cells and their subsequent clearance by macrophages (Mφ). Chronically inflamed sites are characterised by an excess of the key pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) and importantly, TNF-α inhibitors, widely used in the clinical setting for the treatment of rheumatoid arthritis (RA), inflammatory bowel disease and psoriasis, significantly delay disease progression. TNF-α therefore may affect processes implicated in resolution of inflammation. Although TNF-α and pro-inflammatory bacterial products such as lipopolysaccharide (LPS) influence rates of inflammatory cell apoptosis, little is known about their effects on Mφ phagocytosis of apoptotic cells (efferocytosis). In this PhD thesis, the effects of several pro-inflammatory agents (i.e., LPS, lipoteichoic acid (LTA), peptidoglycan (PGN) and TNF-α) on efferocytosis by human blood monocytederived Mφ (MDMφ) have been investigated. LPS, LTA and PGN all inhibited MDMφ efferocytosis in a concentration- and time-dependent manner; however, LPS did not inhibit the uptake of immunoglobulin-G (IgG)-opsonized erythrocytes. Moreover, although TNF-α did inhibit efferocytosis, phagocytosis of IgG-opsonized erythrocytes was not inhibited. Furthermore, the LPS effect was attenuated by dimeric soluble human recombinant TNF receptor-1 (sTNFR1/ Fc), indicating a critical role of TNF-α. Concomitant treatments with monomeric soluble human recombinant TNF receptor-1 (sTNF-R1) or the TNF-α Converting Enzyme (TACE) inhibitor, TOPI-0, only partially reversed the inhibitory effect of LPS. Even though TNF-α release takes place within the first few hours following LPS stimulation, the LPS-induced inhibitory effect occurred only if treatment was performed for 96 hours or longer. Analysis of supernatants obtained from LPS-treated MDMφ revealed that there appears to be interplay between concentrations of TNF-α and interleukin-10 (IL-10) and that these cytokines exert opposing actions on efferocytosis. IL-10 per se increased MDMφ efferocytosis and addition of exogenous IL-10 to LPS-treated samples rescued phagocytosis. The latter effect was associated with the IL-10-induced, concentration-dependent inhibition of TNF-α release. Interestingly, when IL-10 was added to TNF-α-treated MDMφ, only slight augmentation of phagocytosis was observed. Furthermore, when IL-10-mediated effects were blocked by concomitant treatment with anti-human IL-10 receptor 1 antibody (anti-IL-10- R1Ab), the LPS inhibitory effect on phagocytosis was much greater and occurred at 24 hours after treatment. The role of IL-10 on efferocytosis was also investigated using IL-10 deficient murine bone marrow-derived Mφ (BMDMφ). IL-10 deficient BMDMφ, when compared to wild-type, were characterised by a much lower ability to phagocytose apoptotic neutrophils and this effect was independent of culture conditions (control samples and LPS…

Subjects/Keywords: 616.079; phagocytosis; inflammation; macrophages

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APA (6^th Edition):

Michlewska, S. (2011). Macrophage phagocytosis of apoptotic neutrophils is critically regulated by the opposing actions of pro-inflammatory and anti-inflammatory agents : key role for TNF-α. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/5594

Chicago Manual of Style (16^th Edition):

Michlewska, Sylwia. “Macrophage phagocytosis of apoptotic neutrophils is critically regulated by the opposing actions of pro-inflammatory and anti-inflammatory agents : key role for TNF-α.” 2011. Doctoral Dissertation, University of Edinburgh. Accessed February 26, 2020. http://hdl.handle.net/1842/5594.

MLA Handbook (7^th Edition):

Michlewska, Sylwia. “Macrophage phagocytosis of apoptotic neutrophils is critically regulated by the opposing actions of pro-inflammatory and anti-inflammatory agents : key role for TNF-α.” 2011. Web. 26 Feb 2020.

Vancouver:

Michlewska S. Macrophage phagocytosis of apoptotic neutrophils is critically regulated by the opposing actions of pro-inflammatory and anti-inflammatory agents : key role for TNF-α. [Internet] [Doctoral dissertation]. University of Edinburgh; 2011. [cited 2020 Feb 26]. Available from: http://hdl.handle.net/1842/5594.

Council of Science Editors:

Michlewska S. Macrophage phagocytosis of apoptotic neutrophils is critically regulated by the opposing actions of pro-inflammatory and anti-inflammatory agents : key role for TNF-α. [Doctoral Dissertation]. University of Edinburgh; 2011. Available from: http://hdl.handle.net/1842/5594

University of Hawaii – Manoa

24. Killebrew, Deirdre Anne. Activated macrophages: implications in HIV-associated disease pathogenesis.

Degree: PhD, 2009, University of Hawaii – Manoa

URL: http://hdl.handle.net/10125/12107

Electronic reproduction.

Also available by subscription via World Wide Web

xiii, 166 leaves, bound col. ill. 29 cm. +

Subjects/Keywords: HIV infections – Pathogenesis; Macrophages

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APA (6^th Edition):

Killebrew, D. A. (2009). Activated macrophages: implications in HIV-associated disease pathogenesis. (Doctoral Dissertation). University of Hawaii – Manoa. Retrieved from http://hdl.handle.net/10125/12107

Chicago Manual of Style (16^th Edition):

Killebrew, Deirdre Anne. “Activated macrophages: implications in HIV-associated disease pathogenesis.” 2009. Doctoral Dissertation, University of Hawaii – Manoa. Accessed February 26, 2020. http://hdl.handle.net/10125/12107.

MLA Handbook (7^th Edition):

Killebrew, Deirdre Anne. “Activated macrophages: implications in HIV-associated disease pathogenesis.” 2009. Web. 26 Feb 2020.

Vancouver:

Killebrew DA. Activated macrophages: implications in HIV-associated disease pathogenesis. [Internet] [Doctoral dissertation]. University of Hawaii – Manoa; 2009. [cited 2020 Feb 26]. Available from: http://hdl.handle.net/10125/12107.

Council of Science Editors:

Killebrew DA. Activated macrophages: implications in HIV-associated disease pathogenesis. [Doctoral Dissertation]. University of Hawaii – Manoa; 2009. Available from: http://hdl.handle.net/10125/12107

University of Hong Kong

25. 王亮节; Wang, Liangjie. The role of MYC on mycobacterium-induced immune responses in human macrophages.

Degree: PhD, 2016, University of Hong Kong

URL: Wang, L. [王亮节]. (2016). The role of MYC on mycobacterium-induced immune responses in human macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5774067. ; http://dx.doi.org/10.5353/th_b5774067 ; http://hdl.handle.net/10722/238187

published_or_final_version

Paediatrics and Adolescent Medicine

Doctoral

Doctor of Philosophy

Subjects/Keywords: Myc proteins; Myc oncogenes; Macrophages

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APA (6^th Edition):

王亮节; Wang, L. (2016). The role of MYC on mycobacterium-induced immune responses in human macrophages. (Doctoral Dissertation). University of Hong Kong. Retrieved from Wang, L. [王亮节]. (2016). The role of MYC on mycobacterium-induced immune responses in human macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5774067. ; http://dx.doi.org/10.5353/th_b5774067 ; http://hdl.handle.net/10722/238187

Chicago Manual of Style (16^th Edition):

王亮节; Wang, Liangjie. “The role of MYC on mycobacterium-induced immune responses in human macrophages.” 2016. Doctoral Dissertation, University of Hong Kong. Accessed February 26, 2020. Wang, L. [王亮节]. (2016). The role of MYC on mycobacterium-induced immune responses in human macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5774067. ; http://dx.doi.org/10.5353/th_b5774067 ; http://hdl.handle.net/10722/238187.

MLA Handbook (7^th Edition):

王亮节; Wang, Liangjie. “The role of MYC on mycobacterium-induced immune responses in human macrophages.” 2016. Web. 26 Feb 2020.

Vancouver:

王亮节; Wang L. The role of MYC on mycobacterium-induced immune responses in human macrophages. [Internet] [Doctoral dissertation]. University of Hong Kong; 2016. [cited 2020 Feb 26]. Available from: Wang, L. [王亮节]. (2016). The role of MYC on mycobacterium-induced immune responses in human macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5774067. ; http://dx.doi.org/10.5353/th_b5774067 ; http://hdl.handle.net/10722/238187.

Council of Science Editors:

王亮节; Wang L. The role of MYC on mycobacterium-induced immune responses in human macrophages. [Doctoral Dissertation]. University of Hong Kong; 2016. Available from: Wang, L. [王亮节]. (2016). The role of MYC on mycobacterium-induced immune responses in human macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5774067. ; http://dx.doi.org/10.5353/th_b5774067 ; http://hdl.handle.net/10722/238187

University of Hong Kong

26. 陳誠; Chan, Shing. The functional analysis of iron induced microparticles derived from endothelial cells and macrophages.

Degree: PhD, 2014, University of Hong Kong

URL: http://hdl.handle.net/10722/238877

► Iron is an essential element involved in a wide variety of metabolic processes in the body. Accumulation of excessive iron in tissues causes overproduction of… (more)

▼ Iron is an essential element involved in a wide variety of metabolic processes in the body. Accumulation of excessive iron in tissues causes overproduction of superoxide (O2•-) and hydroxyl (OH-) radicals via Fenton and Haber-Weis reactions. Such increased production of reactive oxygen species (ROS) may lead to oxidative stress resulting in cell damage. Clinically, such conditions of iron overload can be found in thalassemia patients with continuous blood transfusions and increased intestinal iron absorption secondary to anemia. It is well known that that iron-overload-induced myocardial damage and systemic arterial dysfunction secondary to endothelial cell damage is a major long term complication in thalassemia patients. When cells undergo activation, injury or apoptosis, cell membrane blebs are formed. Eventually such blebs are evolved into microparticles (MPs) and released. The mechanism of biogenesis of endothelial microparticles (EMPs) by iron overload remains unknown. I found that iron increased the production of ROS and induced mitochondrial damage, as shown by increased calcium levels in mitochondria [〖Ca〗^(2+)]m and loss of mitochondrial membrane potential (ΔΨm). Apoptotic cells were significantly increased under iron treatment. This was associated with increase in activated caspase-3 suggesting that apoptosis was induced via a mitochondria-mediated caspase dependent pathway. My findings suggest that iron overload induced endothelial cells to release EMPs and such release is closely associated with increased oxidative stress, increased [〖Ca〗^(2+)]m, loss of mitochondrial membrane potential and apoptosis of endothelial cells. MPs can serve as vehicle for biological soluble factors involving in the regulation of a wide spectrum of biological functions. Iron overload enhanced tissue factor expression and induced tissue factor-bearing EMPs released from endothelial cells. Furthermore, iron-induced EMPs contain various upregulated miRNA which are associated with cellular senescence, apoptosis, angiogenesis and vascular inflammation. It is interesting that these miRNA-rich EMPs can be taking up by other normal endothelial cell and induced them into apoptosis. It is also interesting that different cells under the same iron overload treatment secrete MPs with different soluble factors which have distinct target cell function. Excessive iron induced MPs releasing from macrophages and they contain tumour necrotic factor- (TNF-). Such TNF- rich MPs enhanced mesenchymal stem cells to differentiate into osteoblasts. This finding explains the possible mechanism of ectopic bone formation at heterotopic ossification site in seriously wounded patients. Finally, I investigated the potential role of interventional agents such as L1, carvedilol in preventing iron-overload-induced cell apoptosis. We found that both L1 and carvedilol inhibited endothelial cell ROS generation, apoptosis, and EMP release. Whether they can prevent iron-overload-induced macrophage secretion of TNF--bearing MPs in the setting of trauma-induced…

Subjects/Keywords: Endothelial cells; Iron - Metabolism; Macrophages

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APA (6^th Edition):

陳誠; Chan, S. (2014). The functional analysis of iron induced microparticles derived from endothelial cells and macrophages. (Doctoral Dissertation). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/238877

Chicago Manual of Style (16^th Edition):

陳誠; Chan, Shing. “The functional analysis of iron induced microparticles derived from endothelial cells and macrophages.” 2014. Doctoral Dissertation, University of Hong Kong. Accessed February 26, 2020. http://hdl.handle.net/10722/238877.

MLA Handbook (7^th Edition):

陳誠; Chan, Shing. “The functional analysis of iron induced microparticles derived from endothelial cells and macrophages.” 2014. Web. 26 Feb 2020.

Vancouver:

陳誠; Chan S. The functional analysis of iron induced microparticles derived from endothelial cells and macrophages. [Internet] [Doctoral dissertation]. University of Hong Kong; 2014. [cited 2020 Feb 26]. Available from: http://hdl.handle.net/10722/238877.

Council of Science Editors:

陳誠; Chan S. The functional analysis of iron induced microparticles derived from endothelial cells and macrophages. [Doctoral Dissertation]. University of Hong Kong; 2014. Available from: http://hdl.handle.net/10722/238877

University of Hong Kong

27. Ling, Wai-lim. A study of the roles of interleukin-17A on macrophage functions in response to mycobacteria infection.

Degree: PhD, 2016, University of Hong Kong

URL: http://hdl.handle.net/10722/239357

published_or_final_version

Paediatrics and Adolescent Medicine

Doctoral

Doctor of Philosophy

Subjects/Keywords: Interleukins; Macrophages; Mycobacterial diseases

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APA (6^th Edition):

Ling, W. (2016). A study of the roles of interleukin-17A on macrophage functions in response to mycobacteria infection. (Doctoral Dissertation). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/239357

Chicago Manual of Style (16^th Edition):

Ling, Wai-lim. “A study of the roles of interleukin-17A on macrophage functions in response to mycobacteria infection.” 2016. Doctoral Dissertation, University of Hong Kong. Accessed February 26, 2020. http://hdl.handle.net/10722/239357.

MLA Handbook (7^th Edition):

Ling, Wai-lim. “A study of the roles of interleukin-17A on macrophage functions in response to mycobacteria infection.” 2016. Web. 26 Feb 2020.

Vancouver:

Ling W. A study of the roles of interleukin-17A on macrophage functions in response to mycobacteria infection. [Internet] [Doctoral dissertation]. University of Hong Kong; 2016. [cited 2020 Feb 26]. Available from: http://hdl.handle.net/10722/239357.

Council of Science Editors:

Ling W. A study of the roles of interleukin-17A on macrophage functions in response to mycobacteria infection. [Doctoral Dissertation]. University of Hong Kong; 2016. Available from: http://hdl.handle.net/10722/239357

University of Hong Kong

28. 黃沛珊; Wong, Bauhinia. Effects of serotonin on LPS- or LTA- stimulated cytokine release in monocytes and macrophages.

Degree: Master of Medical Sciences, 2014, University of Hong Kong

URL: Wong, B. [黃沛珊]. (2014). Effects of serotonin on LPS- or LTA- stimulated cytokine release in monocytes and macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5303984 ; http://dx.doi.org/10.5353/th_b5303984 ; http://hdl.handle.net/10722/206489

►

Chronic obstructive pulmonary disease (COPD) is a progressive disease and characterized by persistent airflow limitation. Pathophysiologically it involves many components, including oxidative stress and inflammation… (more)

▼

Chronic obstructive pulmonary disease (COPD) is a progressive disease and characterized by persistent airflow limitation. Pathophysiologically it involves many components, including oxidative stress and inflammation of the airways and lungs. Although the primary cause of COPD is smoking, acute exacerbation due to infections can accelerate disease progression, which is a significant cause of morbidity, mortality and burden on healthcare costs. One-half of all acute exacerbations of COPD are associated with bacterial infection, with non-typeable Hemophilus influenzae being the most common pathogen. Staphylococcus pneumonia, one of the most common Gram-positive bacterial pathogens, is also involved in airway infections, either primary or subsequent to viral diseases. To COPD patients the common respiratory pathogens include Gram-negative and Gram-positive bacterial species. Lipopolysaccharide (LPS), a major component of the outer membrane of all Gram-negative bacteria, which is the predominant inducer of inflammatory responses, has been widely studied. On the other hand, less is known about Gram-positive bacteria, which do not contain LPS but express lipoteichoic acid (LTA) as an important proinflammatory constituent in their cell wall. Serotonin (5-hydroxytryptamine, 5-HT) is a neurotransmitter that plays an important role in regulating pulmonary function and pathogenesis of inflammation. In this study, we hypothesize that the serotoninergic system may be involved in LPS- and LTA-induced inflammation in COPD. Since monocyte recruitment to lung is a key step in COPD, this study aims to investigate the effects of LPS or LTA alone and in combination of 5-HT pretreatment on the release of pro-inflammatory cytokines in undifferentiated (i.e. monocytes) and differentiated THP-1 cells (i.e. macrophages). LPS, LTA or 5-HT alone induced the release of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) in both monocytes and macrophages. Our findings also showed that 5-HT pretreatment suppressed the LPS-induced IL-8 and MCP-1 release, suggesting that 5-HT might act as an anti-inflammatory mediator. On the other hand, 5-HT pretreatment enhanced the LTA-induced IL-8 and MCP-1 release, indicating that 5-HT might also act as a pro-inflammatory mediator. These results demonstrate that 5-HT may be involved in the differential modulation of inflammatory processes during Gram-negative or Gram-positive infections in COPD.

published_or_final_version

Medicine

Master

Master of Medical Sciences

Subjects/Keywords: Macrophages; Cytokines; Monocytes; Serotonin

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APA (6^th Edition):

黃沛珊; Wong, B. (2014). Effects of serotonin on LPS- or LTA- stimulated cytokine release in monocytes and macrophages. (Masters Thesis). University of Hong Kong. Retrieved from Wong, B. [黃沛珊]. (2014). Effects of serotonin on LPS- or LTA- stimulated cytokine release in monocytes and macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5303984 ; http://dx.doi.org/10.5353/th_b5303984 ; http://hdl.handle.net/10722/206489

Chicago Manual of Style (16^th Edition):

黃沛珊; Wong, Bauhinia. “Effects of serotonin on LPS- or LTA- stimulated cytokine release in monocytes and macrophages.” 2014. Masters Thesis, University of Hong Kong. Accessed February 26, 2020. Wong, B. [黃沛珊]. (2014). Effects of serotonin on LPS- or LTA- stimulated cytokine release in monocytes and macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5303984 ; http://dx.doi.org/10.5353/th_b5303984 ; http://hdl.handle.net/10722/206489.

MLA Handbook (7^th Edition):

黃沛珊; Wong, Bauhinia. “Effects of serotonin on LPS- or LTA- stimulated cytokine release in monocytes and macrophages.” 2014. Web. 26 Feb 2020.

Vancouver:

黃沛珊; Wong B. Effects of serotonin on LPS- or LTA- stimulated cytokine release in monocytes and macrophages. [Internet] [Masters thesis]. University of Hong Kong; 2014. [cited 2020 Feb 26]. Available from: Wong, B. [黃沛珊]. (2014). Effects of serotonin on LPS- or LTA- stimulated cytokine release in monocytes and macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5303984 ; http://dx.doi.org/10.5353/th_b5303984 ; http://hdl.handle.net/10722/206489.

Council of Science Editors:

黃沛珊; Wong B. Effects of serotonin on LPS- or LTA- stimulated cytokine release in monocytes and macrophages. [Masters Thesis]. University of Hong Kong; 2014. Available from: Wong, B. [黃沛珊]. (2014). Effects of serotonin on LPS- or LTA- stimulated cytokine release in monocytes and macrophages. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5303984 ; http://dx.doi.org/10.5353/th_b5303984 ; http://hdl.handle.net/10722/206489

University of Hong Kong

29. Dutry, Isabelle Cecile Angele. Susceptibility of human macrophages to influenza A infection.

Degree: PhD, 2012, University of Hong Kong

URL: Dutry, I. C. A.. (2012). Susceptibility of human macrophages to influenza A infection. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4979947 ; http://dx.doi.org/10.5353/th_b4979947 ; http://hdl.handle.net/10722/181513

► The seasonal Influenza A viruses are respiratory pathogens causing epidemics annually with mild illnesses, while sporadically, novel influenza viruses emerge and trigger pandemics associated with… (more)

▼ The seasonal Influenza A viruses are respiratory pathogens causing epidemics annually with mild illnesses, while sporadically, novel influenza viruses emerge and trigger pandemics associated with more widespread and sometimes severe disease. The biological basis for severity of influenza disease remains unclear though it is recognized that the interplay between the influenza viruses and the host immune responses both contribute to viral pathogenesis. As macrophages are key sentinels of the innate immune response and play a crucial role in being the “first responders” as well as contributing to shaping the subsequent (pathogen‐specific) adaptive immune response, the objective of this research was to bring insights on the outcomes of the interactions of influenza viruses with the macrophages. The occurrence of Antibody‐Dependent Enhancement (ADE) of Influenza infection in macrophages was investigated. ADE occurs when non‐neutralized virus‐antibody complexes find alternative entry routes into host cells, mainly through the Fc‐receptor pathway and has been demonstrated predominantly in macrophages. Addition of human serum from some individuals to influenza A virus (either H5 pseudoparticles or pandemic (H1N1) virus) led to enhanced infection of murine macrophage‐like cells as illustrated by a two to five fold increase in detection of influenza M‐gene copies. Immunofluorescence microscopy indicated that serum‐mediated pandemic (H1N1) infection led to an increase in the number of infected cells than in controls. As the fold change in viral gene copies paralleled the fold increase of infected cells I concluded that ADE infection provide pandemic (H1N1) virus with increased opportunity to infect cells rather than simply increase the viral load per cell. In order to strengthen our results, and make them more physiologically relevant, experiments were then performed with human primary cells with clinical sera. However, ADE was not demonstrated in primary human macrophages, suggesting that ADE may be cell type or host specific. The second research question investigated was whether the different state of human primary macrophage differentiation or activation in vitro determined the susceptibility to influenza infection. Recently, work by others has shown a diverse range of macrophage phenotypes that arise by differences in macrophage differentiation and activation. In addition to the classical activation pathway (caMΦ), new mechanisms of activation, designated as alternative activation (aaMΦ), have been reported. Classically and alternatively activated macrophages display different phenotypes and properties, such as molecule expression patterns, cytokine secretion, and gene signatures. This study constitutes the first systematic comparison of Influenza A virus infection of these different subsets of human primary monocyte‐derived macrophages. When assessed for their permissiveness to different influenza A viruses, aaMΦΦshowed greater susceptibility to influenza A infection than caMΦ. This work also documents the receptor… Advisors/Committee Members: Peiris, JSM.

Subjects/Keywords: Influenza A virus.; Macrophages.

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APA (6^th Edition):

Dutry, I. C. A. (2012). Susceptibility of human macrophages to influenza A infection. (Doctoral Dissertation). University of Hong Kong. Retrieved from Dutry, I. C. A.. (2012). Susceptibility of human macrophages to influenza A infection. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4979947 ; http://dx.doi.org/10.5353/th_b4979947 ; http://hdl.handle.net/10722/181513

Chicago Manual of Style (16^th Edition):

Dutry, Isabelle Cecile Angele. “Susceptibility of human macrophages to influenza A infection.” 2012. Doctoral Dissertation, University of Hong Kong. Accessed February 26, 2020. Dutry, I. C. A.. (2012). Susceptibility of human macrophages to influenza A infection. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4979947 ; http://dx.doi.org/10.5353/th_b4979947 ; http://hdl.handle.net/10722/181513.

MLA Handbook (7^th Edition):

Dutry, Isabelle Cecile Angele. “Susceptibility of human macrophages to influenza A infection.” 2012. Web. 26 Feb 2020.

Vancouver:

Dutry ICA. Susceptibility of human macrophages to influenza A infection. [Internet] [Doctoral dissertation]. University of Hong Kong; 2012. [cited 2020 Feb 26]. Available from: Dutry, I. C. A.. (2012). Susceptibility of human macrophages to influenza A infection. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4979947 ; http://dx.doi.org/10.5353/th_b4979947 ; http://hdl.handle.net/10722/181513.

Council of Science Editors:

Dutry ICA. Susceptibility of human macrophages to influenza A infection. [Doctoral Dissertation]. University of Hong Kong; 2012. Available from: Dutry, I. C. A.. (2012). Susceptibility of human macrophages to influenza A infection. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4979947 ; http://dx.doi.org/10.5353/th_b4979947 ; http://hdl.handle.net/10722/181513

University of Aberdeen

30. McKenzie, Christopher Gordon Jemison. Candida albicans recognition by and escape from macrophages.

Degree: 2011, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=167784 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.542642

► Disruption of N-mannosylation and O-mannosylation on the C. albicans outer cell wall increased the rate by which C. albicans is ingested by macrophages. Conversely, disruption… (more)

Subjects/Keywords: 616.9; Candida Albicans : Macrophages

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

APA (6^th Edition):

McKenzie, C. G. J. (2011). Candida albicans recognition by and escape from macrophages. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=167784 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.542642

Chicago Manual of Style (16^th Edition):

McKenzie, Christopher Gordon Jemison. “Candida albicans recognition by and escape from macrophages.” 2011. Doctoral Dissertation, University of Aberdeen. Accessed February 26, 2020. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=167784 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.542642.

MLA Handbook (7^th Edition):

McKenzie, Christopher Gordon Jemison. “Candida albicans recognition by and escape from macrophages.” 2011. Web. 26 Feb 2020.

Vancouver:

McKenzie CGJ. Candida albicans recognition by and escape from macrophages. [Internet] [Doctoral dissertation]. University of Aberdeen; 2011. [cited 2020 Feb 26]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=167784 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.542642.

Council of Science Editors:

McKenzie CGJ. Candida albicans recognition by and escape from macrophages. [Doctoral Dissertation]. University of Aberdeen; 2011. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=167784 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.542642

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