subject:(Immunology AND Infectious Disease)

McMaster University

1. D'Agostino, Michael. Investigating the role of memory alveolar macrophages in early innate immune control of pulmonary tuberculosis.

Degree: MSc, 2019, McMaster University

URL: http://hdl.handle.net/11375/24846

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Mycobacterium tuberculosis (M.tb) is the causative agent of pulmonary tuberculosis (TB). Over 25% of the world’s population is estimated to be infected with tuberculosis, yielding… (more)

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Mycobacterium tuberculosis (M.tb) is the causative agent of pulmonary tuberculosis (TB). Over 25% of the world’s population is estimated to be infected with tuberculosis, yielding over 10 million new cases and over 1.5 million deaths in 2017 alone. This is all despite the near universal implementation of bacille Calmette-Guérin (BCG) vaccination across TB endemic areas. BCG is capable of preventing childhood disseminated forms of disease but fails to induce potent immunity within the lung. We expect this to in part play a role in the lack of protection against pulmonary TB. Our lab has developed a human adenovirus serotype 5 vaccine expressing the M.tb antigen Ag85A (AdHu5Ag85A). When delivered directly to the respiratory mucosa (RM), AdHu5Ag85A has proven to be safe and immunogenic, generating both CD4 and CD8 T cell responses within the lung. We have found that RM AdHu5Ag85A vaccination also generates a long-lasting population of memory macrophages in the airway and lung, that are primed to better control early M.tb infection. Importantly, this was a vaccination route-dependent mechanism. Memory macrophages express a trained innate immune phenotype as they express high levels of MHC II, are highly glycolytic, and produce more IL-12 upon re-stimulation. Importantly, utilization of an in vivo T cell depletion approach allowed us to show that these memory macrophages are capable of limiting early M.tb infection independent of T cells. Our findings indicate that RM vaccination may be advantageous to parenteral routes by not only drawing antigen specific T cells into immunologically restricted lung mucosa but also generating a memory macrophage population within the lung. Induction of memory macrophages within the airway helps overcome early innate immune suppression by M.tb.

Thesis

Master of Health Sciences (MSc)

Tuberculosis (TB) is a pulmonary disease responsible for 10 million new clinical cases and more than 1 million deaths annually. Over one quarter of the world is believed to be infected with TB. This is despite the near-universal administration of bacille Calmette-Guérin, a preventative TB vaccine, and an effective, but lengthy antibiotic treatment. With antibiotic resistance on the rise, developing a protective vaccine against TB is more important than ever. Tuberculosis has confounded researchers for decades and has thus escaped development of a more effective vaccine. One of the ways to improve a TB vaccine would be to inhale it, to have local effects at the main site of TB infection in the lung. We found that by aerosolizing our vaccine, we can impact local immunity within the lung in a way that has never before been described, opening new avenues for TB research.

Advisors/Committee Members: Xing, Zhou, Medical Sciences.

Subjects/Keywords: Immunology; Infectious disease

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APA (6^th Edition):

D'Agostino, M. (2019). Investigating the role of memory alveolar macrophages in early innate immune control of pulmonary tuberculosis. (Masters Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/24846

Chicago Manual of Style (16^th Edition):

D'Agostino, Michael. “Investigating the role of memory alveolar macrophages in early innate immune control of pulmonary tuberculosis.” 2019. Masters Thesis, McMaster University. Accessed February 25, 2020. http://hdl.handle.net/11375/24846.

MLA Handbook (7^th Edition):

D'Agostino, Michael. “Investigating the role of memory alveolar macrophages in early innate immune control of pulmonary tuberculosis.” 2019. Web. 25 Feb 2020.

Vancouver:

D'Agostino M. Investigating the role of memory alveolar macrophages in early innate immune control of pulmonary tuberculosis. [Internet] [Masters thesis]. McMaster University; 2019. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/11375/24846.

Council of Science Editors:

D'Agostino M. Investigating the role of memory alveolar macrophages in early innate immune control of pulmonary tuberculosis. [Masters Thesis]. McMaster University; 2019. Available from: http://hdl.handle.net/11375/24846

University of Louisville

2. Hutcherson, Justin. Characterization of the innate response to the RagB protein of Porphyromonas gingivalis.

Degree: PhD, 2015, University of Louisville

URL: 10.18297/etd/2077 ; https://ir.library.louisville.edu/etd/2077

► More than 64 million people in the US suffer from some form of periodontal disease. Periodontal diseases are bacterial infections of the hard and… (more)

Subjects/Keywords: Immunology and Infectious Disease; Microbiology

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APA (6^th Edition):

Hutcherson, J. (2015). Characterization of the innate response to the RagB protein of Porphyromonas gingivalis. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/2077 ; https://ir.library.louisville.edu/etd/2077

Chicago Manual of Style (16^th Edition):

Hutcherson, Justin. “Characterization of the innate response to the RagB protein of Porphyromonas gingivalis.” 2015. Doctoral Dissertation, University of Louisville. Accessed February 25, 2020. 10.18297/etd/2077 ; https://ir.library.louisville.edu/etd/2077.

MLA Handbook (7^th Edition):

Hutcherson, Justin. “Characterization of the innate response to the RagB protein of Porphyromonas gingivalis.” 2015. Web. 25 Feb 2020.

Vancouver:

Hutcherson J. Characterization of the innate response to the RagB protein of Porphyromonas gingivalis. [Internet] [Doctoral dissertation]. University of Louisville; 2015. [cited 2020 Feb 25]. Available from: 10.18297/etd/2077 ; https://ir.library.louisville.edu/etd/2077.

Council of Science Editors:

Hutcherson J. Characterization of the innate response to the RagB protein of Porphyromonas gingivalis. [Doctoral Dissertation]. University of Louisville; 2015. Available from: 10.18297/etd/2077 ; https://ir.library.louisville.edu/etd/2077

University of Louisville

3. Camp, Jeremy V., 1980-. Critical insights into the pathogenesis of clinical isolates of pandemic influenza A(H1N1) 2009 virus in mouse and ferret models.

Degree: PhD, 2015, University of Louisville

URL: 10.18297/etd/2079 ; https://ir.library.louisville.edu/etd/2079

► Influenza A virus (IAV) is a minus-sense, segmented, single-stranded RNA virus that infects the respiratory tract of humans and can cause severe illness. Novel… (more)

▼ Influenza A virus (IAV) is a minus-sense, segmented, single-stranded RNA virus that infects the respiratory tract of humans and can cause severe illness. Novel IAV variants perpetually emerge on every continent, and the emergence of variants with increased transmissibility and/or pathogenesis in the human population is a serious concern for global public health. Infection with IAV typically causes an acute, self-limiting upper respiratory tract disease. However, severe IAV disease is characterized by infection of the lower respiratory tract which can lead to pneumonia and may result in the development of acute respiratory distress syndrome (ARDS). Viral and host contributions to the development of ARDS are poorly understood, however IAV pathogenesis has been linked mutations in the receptor binding protein and the viral polymerase. Ferrets and mice are two important laboratory animal models for studying IAV pathogenesis. In 2009, a novel H1N1 subtype IAV (H1N1pdm) emerged in the human population and displayed variable pathology in humans. Using a mouse model, we show the variability of clinical isolates of H1N1pdm is driven by viral mutations, and that the timing of the inflammatory response is correlated with disease severity. To investigate spatiotemporal aspects of potential host and viral contributions to influenza pathogenesis, we developed a live imaging platform for ferrets infected with a human clinical isolate of H1N1pdm. We detected an early recruitment of neutrophils into ferret lungs following infection, which accumulated at foci of H1N1pdm infection within specific anatomical regions of the lung by 24 hours post-infection. The neutrophil response was biphasic, characterized by the recruitment of two populations with differing gene expression profiles, and baseline neutrophil levels were increased throughout the entire lung, including areas with no apparent viral infection. Changes in the viral microenvironment resulted in the regeneration of lung epithelium during recovery phase of infection, and this was imaged with PET-CT using a radiolabeled glucose analog. In summary, these data illustrate critical features of the immune response to IAV, and emphasize important considerations about the timing and accuracy of innate immune responses in studying viral pathogenesis. Advisors/Committee Members: Jonsson, Colleen B., Fraig, Mostafa, Lawrenz, Matthew, Mitchell, Thomas, Uriarte, Silvia.

Subjects/Keywords: Immunology and Infectious Disease; Microbiology

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APA (6^th Edition):

Camp, Jeremy V., 1. (2015). Critical insights into the pathogenesis of clinical isolates of pandemic influenza A(H1N1) 2009 virus in mouse and ferret models. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/2079 ; https://ir.library.louisville.edu/etd/2079

Chicago Manual of Style (16^th Edition):

Camp, Jeremy V., 1980-. “Critical insights into the pathogenesis of clinical isolates of pandemic influenza A(H1N1) 2009 virus in mouse and ferret models.” 2015. Doctoral Dissertation, University of Louisville. Accessed February 25, 2020. 10.18297/etd/2079 ; https://ir.library.louisville.edu/etd/2079.

MLA Handbook (7^th Edition):

Camp, Jeremy V., 1980-. “Critical insights into the pathogenesis of clinical isolates of pandemic influenza A(H1N1) 2009 virus in mouse and ferret models.” 2015. Web. 25 Feb 2020.

Vancouver:

Camp, Jeremy V. 1. Critical insights into the pathogenesis of clinical isolates of pandemic influenza A(H1N1) 2009 virus in mouse and ferret models. [Internet] [Doctoral dissertation]. University of Louisville; 2015. [cited 2020 Feb 25]. Available from: 10.18297/etd/2079 ; https://ir.library.louisville.edu/etd/2079.

Council of Science Editors:

Camp, Jeremy V. 1. Critical insights into the pathogenesis of clinical isolates of pandemic influenza A(H1N1) 2009 virus in mouse and ferret models. [Doctoral Dissertation]. University of Louisville; 2015. Available from: 10.18297/etd/2079 ; https://ir.library.louisville.edu/etd/2079

University of Louisville

4. Gerlach, Rachael Lask. Early host response and immune signaling to 2009 pandemic influenza A (H1N1) viruses in primary cell culture models.

Degree: PhD, 2015, University of Louisville

URL: 10.18297/etd/2078 ; https://ir.library.louisville.edu/etd/2078

► Influenza A virus (IAV) subtypes and even genotypes within subtypes can show differences in tropism (host, cell type), magnitude of infection, immune response and… (more)

▼ Influenza A virus (IAV) subtypes and even genotypes within subtypes can show differences in tropism (host, cell type), magnitude of infection, immune response and progression of illness. My dissertation focused on the development and use of two in vitro physiologically-relevant human cell culture models, well-differentiated normal human bronchial epithelial (wdNHBE) cells and human monocyte-derived macrophages (MDM) for the study of early IAV-host interactions. These models have given new insight into early host responses to seasonal H1N1 (BN59) and two pandemic A(H1N1)2009 viruses or H1N1pdm herein. The H1N1pdm are clinical isolates from a fatal (A/KY/180/10) and nonfatal (A/KY/136/09) case. In the wdNHBE model, KY180 showed a significantly higher titer as compared to the other two viruses at 24 hpi (hours post-infection). Interestingly, by microarray analysis, there were no significant differences in the host genome-wide expression intensity profiles of each virus following infection. Soluble cytokine measurements revealed increased apical and basal pro-inflammatory cytokine secretion overtime. A key finding from our data was greater basolateral secretion of cytokines (IL6, CCL5, CCL4 and CCL2) by KY180-infected wdNHBE cells. This finding suggests that the basolateral signals from infected epithelial cells may differ in their potential for recruitment and responses elicited by recruited monocytes/macrophages. In the second model, I used an in vitro model of recruited “resting” MDMs to study virus-host interactions of the clinical H1N1pdm isolates. These viruses replicated in MDM albeit inefficiently. While titers were similar and remained relatively low for all isolates, pro- and anti-inflammatory expression levels differed markedly between KY180 as compared to KY136 and BN59. KY180 had delayed expression at 8 hpi of pro-inflammatory genes (CCL5, TNF, IFN, CXCL10). This apparent delay in response to KY180 depended on the mode of viral entry. For KY180, this occurred primarily through macropinocytosis, mapping to the HA1 gene. In summary, my studies reveal subtle, yet important differences in IAV-host interactions that result in alterations of immune signaling in epithelial and macrophage cell culture models. Continued advancement of the in vitro human cell culture models for the study of IAV is important as they will allow mechanistic insight into the intricate biology of these viruses. Advisors/Committee Members: Jonsson, Colleen B., Bodduluri, Haribabu, Kosiewicz, Michele, Lukashevich, Igor, Shirwan, Haval, Suttles, Jill.

Subjects/Keywords: Immunology and Infectious Disease; Microbiology

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

APA (6^th Edition):

Gerlach, R. L. (2015). Early host response and immune signaling to 2009 pandemic influenza A (H1N1) viruses in primary cell culture models. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/2078 ; https://ir.library.louisville.edu/etd/2078

Chicago Manual of Style (16^th Edition):

Gerlach, Rachael Lask. “Early host response and immune signaling to 2009 pandemic influenza A (H1N1) viruses in primary cell culture models.” 2015. Doctoral Dissertation, University of Louisville. Accessed February 25, 2020. 10.18297/etd/2078 ; https://ir.library.louisville.edu/etd/2078.

MLA Handbook (7^th Edition):

Gerlach, Rachael Lask. “Early host response and immune signaling to 2009 pandemic influenza A (H1N1) viruses in primary cell culture models.” 2015. Web. 25 Feb 2020.

Vancouver:

Gerlach RL. Early host response and immune signaling to 2009 pandemic influenza A (H1N1) viruses in primary cell culture models. [Internet] [Doctoral dissertation]. University of Louisville; 2015. [cited 2020 Feb 25]. Available from: 10.18297/etd/2078 ; https://ir.library.louisville.edu/etd/2078.

Council of Science Editors:

Gerlach RL. Early host response and immune signaling to 2009 pandemic influenza A (H1N1) viruses in primary cell culture models. [Doctoral Dissertation]. University of Louisville; 2015. Available from: 10.18297/etd/2078 ; https://ir.library.louisville.edu/etd/2078

University of Louisville

5. Zhu, Yanfang. Regulation of macrophage inflammatory signaling pathways by AMP-activated protein kinase.

Degree: PhD, 2014, University of Louisville

URL: 10.18297/etd/1649 ; https://ir.library.louisville.edu/etd/1649

► AMP-activated protein kinase, AMPK, is a conserved serine/threonine kinase with a critical function in the regulation of metabolic pathways in eukaryotic cells. Recently, AMPK… (more)

▼ AMP-activated protein kinase, AMPK, is a conserved serine/threonine kinase with a critical function in the regulation of metabolic pathways in eukaryotic cells. Recently, AMPK has been shown to play an additional role as a regulator of inflammatory activity in leukocytes. Treatment of macrophages with chemical AMPK activators, or forced expression of a constitutively active form of AMPK, results in polarization to an antiinflammatory phenotype. Additionally, we reported previously that stimulation of macrophages with antiinflammatory cytokines such as IL-10, IL-4 and TGF-ß results in rapid activation of AMPK, suggesting that AMPK contributes to the suppressive function of these cytokines. In the current study we investigated the role of AMPK in the regulation of macrophage antiatherogenic functions and demonstrated a new mechanism for AMPK’s role in mediating IL-10-induced gene expression and antiinflammatory effects. The expression of dominant negative (DN-) AMPKa1 in macrophages resulted in a spontaneous obese phenotype in mice associated with fatty liver and heart enlargement. The expression of constitutively active (CA-) AMPKa1 in macrophages resulted in decreased IL-6 production but increased expression of ABCA1 and ApoE. Compared to wild-type macrophages, AMPKa1-deficient macrophages failed to express atheroprotective genes including ApoE, LXRa, and ABCA1 in response to IL-10. Mechanistic studies revealed that IL-10-stimulated wild-type macrophages displayed rapid activation of PI3K and its downstream target Akt, an effect that was not seen in macrophages generated from AMPKa1-deficient mice. Treatment with the PI3K inhibitor LY294002 blocked IL-10’s ability to induce Akt activation but not AMPK activation, suggesting that IL-10-mediated activation of AMPK is independent of PI3K. CA-AMPKa1 macrophages displayed elevated PI3K and CREB activation in response to IL-10 compared to the empty vector transfected macrophages. IL-10 stimulation resulted in increased mTORC1 activity, an Akt downstream target, an effect that was reduced in AMPKa1-deficient mice. IL-10 induced phosphorylation of both Tyr705 and Ser727 residues of STAT3 in an AMPKa1-dependent manner, and these phosphorylation events were blocked by inhibition of CaMKKß, an upstream activator of AMPK, and by the mTORC1 inhibitor rapamycin, respectively. The impaired STAT3 phosphorylation in response to IL-10 observed in AMPKa1-deficient macrophages was accompanied by reduced SOCS3 expression and an inadequacy of IL-10 to suppress LPS-induced proinflammatory cytokine production. Overall, our data demonstrate that AMPKa1 is required for IL-10 activation of the PI3K/Akt/mTORC1 and STAT3/SOCS3 antiinflammatory pathways regulating macrophage polarization, a mechanism with broad-reaching applicability in immune homeostasis and in inflammation-associated diseases such as atherosclerosis, autoimmune diseases, and obesity. Advisors/Committee Members: Suttles, Jill.

Subjects/Keywords: Immunology and Infectious Disease; Microbiology

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

APA (6^th Edition):

Zhu, Y. (2014). Regulation of macrophage inflammatory signaling pathways by AMP-activated protein kinase. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/1649 ; https://ir.library.louisville.edu/etd/1649

Chicago Manual of Style (16^th Edition):

Zhu, Yanfang. “Regulation of macrophage inflammatory signaling pathways by AMP-activated protein kinase.” 2014. Doctoral Dissertation, University of Louisville. Accessed February 25, 2020. 10.18297/etd/1649 ; https://ir.library.louisville.edu/etd/1649.

MLA Handbook (7^th Edition):

Zhu, Yanfang. “Regulation of macrophage inflammatory signaling pathways by AMP-activated protein kinase.” 2014. Web. 25 Feb 2020.

Vancouver:

Zhu Y. Regulation of macrophage inflammatory signaling pathways by AMP-activated protein kinase. [Internet] [Doctoral dissertation]. University of Louisville; 2014. [cited 2020 Feb 25]. Available from: 10.18297/etd/1649 ; https://ir.library.louisville.edu/etd/1649.

Council of Science Editors:

Zhu Y. Regulation of macrophage inflammatory signaling pathways by AMP-activated protein kinase. [Doctoral Dissertation]. University of Louisville; 2014. Available from: 10.18297/etd/1649 ; https://ir.library.louisville.edu/etd/1649

Loyola University Chicago

6. Krukowski, Karen. Psychosocial Distress Mediates Immune Dysregulation Through Alterations in Global Epigenetic Patterns and Chromatin Remodeling Proteins.

Degree: PhD, Microbiology and Immunology, 2013, Loyola University Chicago

URL: https://ecommons.luc.edu/luc_diss/525

► Psychosocial distress, characterized by increased perceived stress, anxiety and mood disturbance, is a common response of women to a diagnosis of breast cancer (Northouse,… (more)

▼ Psychosocial distress, characterized by increased perceived stress, anxiety and mood disturbance, is a common response of women to a diagnosis of breast cancer (Northouse, 1992; Pettingale et al., 1988; Stark and House, 2000; Witek-Janusek et al., 2007). This psychosocial distress leads to activation of the hypothalamic-pituitary-adrenocortical (HPA) axis and increased circulating glucocorticoids (GCs) (Chrousos, 2000; Chrousos and Gold, 1992; Schoneveld and Cidlowski, 2007). Increased psychosocial distress and increased HPA activation can lead to immune dysregulation consisting of reduced natural killer (NK) cell activity (NKCA) (Biondi, 2001; Kiecolt-Glaser et al., 1987; Kiecolt-Glaser et al., 2002; Witek-Janusek et al., 2008; Witek-Janusek et al., 2007). This is of particular relevance to women with breast cancer as altered immune cell function is important for tumor control (Curcio et al., 2003; D'Anello et al., 2010; Diefenbach and Raulet, 2002; Hartman et al., 2011; Kishimoto, 2005; Knupfer and Preiss, 2007; Street et al., 2001; van den Broek et al., 1996). The psychological distress in response to a diagnosis of breast cancer diagnosis has relevance for women with breast cancer, as it may contribute to poor cancer outcome. Yet little is known about the molecular mechanism(s) by which psychosocial distress results in NK cell dysregulation. The overall purpose of this project was to evaluate a potential mechanism posited to underlie altered NK cell function observed in women with breast cancer. Increased psychosocial distress increases GCs like cortisol which can impact NK cell function; therefore cortisol levels were measured. Morning cortisol rise inversely correlated with NKCA, such that women with decreased NKCA exhibited an elevation in the morning cortisol rise. Additionally, in vitro treatment of a human NK cell line, NK92 cells, treated with a synthetic GC (dexamethasone) resulted in decreased NKCA. Together these results suggest that cortisol altered lytic function of NK cells. As GCs have been shown to alter cell function by altering epigenetic patterns, global histone modifications were investigated. In both ex vivo analysis of NK cells derived from peripheral blood of women with breast cancer and NK92 cells treated with GCs significant reductions in global acetylation of histone 4 lysine 8 (H4-K8-Ac) were observed, when compared to the age-matched Control women or untreated NK92 cells, respectively. These reductions in H4-K8-Ac correlated with NK cell lytic function as measured by NKCA and intracellular perforin levels in NK cells. Further others show GCs alter epigenetic patterns through recruitment of HDACs, thus this was investigated. Findings show decreased global H4-K8-Ac patterns in NK cells were associated with increased nuclear localization of HDAC2, suggesting that GCs recruit HDAC2 into the nucleus causing decreased global H4-K8-Ac and NKCA. These data identify decreased global H4-K8-Ac and increased nuclear localization of HDAC2 as potential markers of decreased NK cell lytic…

Subjects/Keywords: Immunology and Infectious Disease

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

APA (6^th Edition):

Krukowski, K. (2013). Psychosocial Distress Mediates Immune Dysregulation Through Alterations in Global Epigenetic Patterns and Chromatin Remodeling Proteins. (Doctoral Dissertation). Loyola University Chicago. Retrieved from https://ecommons.luc.edu/luc_diss/525

Chicago Manual of Style (16^th Edition):

Krukowski, Karen. “Psychosocial Distress Mediates Immune Dysregulation Through Alterations in Global Epigenetic Patterns and Chromatin Remodeling Proteins.” 2013. Doctoral Dissertation, Loyola University Chicago. Accessed February 25, 2020. https://ecommons.luc.edu/luc_diss/525.

MLA Handbook (7^th Edition):

Krukowski, Karen. “Psychosocial Distress Mediates Immune Dysregulation Through Alterations in Global Epigenetic Patterns and Chromatin Remodeling Proteins.” 2013. Web. 25 Feb 2020.

Vancouver:

Krukowski K. Psychosocial Distress Mediates Immune Dysregulation Through Alterations in Global Epigenetic Patterns and Chromatin Remodeling Proteins. [Internet] [Doctoral dissertation]. Loyola University Chicago; 2013. [cited 2020 Feb 25]. Available from: https://ecommons.luc.edu/luc_diss/525.

Council of Science Editors:

Krukowski K. Psychosocial Distress Mediates Immune Dysregulation Through Alterations in Global Epigenetic Patterns and Chromatin Remodeling Proteins. [Doctoral Dissertation]. Loyola University Chicago; 2013. Available from: https://ecommons.luc.edu/luc_diss/525

Loyola University Chicago

7. Nomellini, Vanessa. Aging Effects on Acute Lung Inflammation After Burn Injury.

Degree: PhD, Molecular and Cellular Biochemistry Program, 2010, Loyola University Chicago

URL: https://ecommons.luc.edu/luc_diss/144

► The risk of complications and death after a moderate sized burn injury is significantly higher in persons over the age of 65, while almost… (more)

▼ The risk of complications and death after a moderate sized burn injury is significantly higher in persons over the age of 65, while almost non-existant in young, healthy individuals. The studies outlined below use a murine model to determine the mechanisms behind the development of pulmonary complications that frequently occur in aged individuals following burn injury. We hypothesized that, since aged mice maintain an elevated proinflammatory state prior to injury, they are at an even greater risk of pulmonary inflammation than young mice given a comparable sized wound. We found that neutrophils continue to accumulate in the lungs of aged mice at 24 hours after burn injury, but do not migrate into the alveoli. We also showed that neutrophil migration towards KC – a dominant neutrophil chemokine – in a transwell chemotaxis assay is robust in neutrophils from young mice, but blunted in those from aged mice. These differences are likely due to intracellular signaling defects, as levels of the receptor for KC, CXCR2, is not different on neutrophils between age groups. In addition, we found that burn injury causes a significant decrease in CXCR2 on the surface of neutrophils, indicating that these cells are more susceptible to receptor desensitization. When anti-CXCR2 antibody is injected immediately post-burn, the aberrant pulmonary inflammation is completely abolished in aged mice compared to those receiving a control antibody, suggesting that targeting this pathway in the acute stages of burn help dampen the inflammatory response of the aged mice. In a separate set of experiments, we demonstrated that expression of the cell adhesion molecule, ICAM-1, on pulmonary vasculature and non-specific neutrophil adhesion is increased in aged mice following burn injury. In sum, we concluded that neutrophils accumulate in the lungs of aged mice as a result of sequestration in the pulmonary vasculature due to defective CXCR2-mediated migration and increased adhesion. These studies are critical to understanding why aged patients are at such a higher risk for pulmonary complications after burn injury and reveal targets for new and better therapeutic regimens that could potentially help older patients reach full recovery.

Subjects/Keywords: Immunology and Infectious Disease

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

APA (6^th Edition):

Nomellini, V. (2010). Aging Effects on Acute Lung Inflammation After Burn Injury. (Doctoral Dissertation). Loyola University Chicago. Retrieved from https://ecommons.luc.edu/luc_diss/144

Chicago Manual of Style (16^th Edition):

Nomellini, Vanessa. “Aging Effects on Acute Lung Inflammation After Burn Injury.” 2010. Doctoral Dissertation, Loyola University Chicago. Accessed February 25, 2020. https://ecommons.luc.edu/luc_diss/144.

MLA Handbook (7^th Edition):

Nomellini, Vanessa. “Aging Effects on Acute Lung Inflammation After Burn Injury.” 2010. Web. 25 Feb 2020.

Vancouver:

Nomellini V. Aging Effects on Acute Lung Inflammation After Burn Injury. [Internet] [Doctoral dissertation]. Loyola University Chicago; 2010. [cited 2020 Feb 25]. Available from: https://ecommons.luc.edu/luc_diss/144.

Council of Science Editors:

Nomellini V. Aging Effects on Acute Lung Inflammation After Burn Injury. [Doctoral Dissertation]. Loyola University Chicago; 2010. Available from: https://ecommons.luc.edu/luc_diss/144

8. Hendrix, Emily K. Characterizing the early stages of a novel host shift using host fitness and metabolomics.

Degree: MS, Biology, 2018, Eastern Washington University

URL: https://dc.ewu.edu/theses/500

► The factors that contribute to successful colonization of a novel host species by a pathogen remain unclear. One likely factor determining host shift success… (more)

Subjects/Keywords: Biology; Immunology of Infectious Disease

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APA (6^th Edition):

Hendrix, E. K. (2018). Characterizing the early stages of a novel host shift using host fitness and metabolomics. (Thesis). Eastern Washington University. Retrieved from https://dc.ewu.edu/theses/500

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):

Hendrix, Emily K. “Characterizing the early stages of a novel host shift using host fitness and metabolomics.” 2018. Thesis, Eastern Washington University. Accessed February 25, 2020. https://dc.ewu.edu/theses/500.

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

MLA Handbook (7^th Edition):

Hendrix, Emily K. “Characterizing the early stages of a novel host shift using host fitness and metabolomics.” 2018. Web. 25 Feb 2020.

Vancouver:

Hendrix EK. Characterizing the early stages of a novel host shift using host fitness and metabolomics. [Internet] [Thesis]. Eastern Washington University; 2018. [cited 2020 Feb 25]. Available from: https://dc.ewu.edu/theses/500.

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

Council of Science Editors:

Hendrix EK. Characterizing the early stages of a novel host shift using host fitness and metabolomics. [Thesis]. Eastern Washington University; 2018. Available from: https://dc.ewu.edu/theses/500

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

Loyola University Chicago

9. Bush, Kristin. Role for Histone Deacetylases in Glucocorticoid Receptor Mediated Transpression of Natural Killer Cell Activity.

Degree: MS, Microbiology and Immunology, 2011, Loyola University Chicago

URL: http://ecommons.luc.edu/luc_theses/567

► During periods of psychosocial distress glucocorticoids (GCs) are known to reduce the lytic activity of natural killer cells (NKCA). Glucocorticoid treatment also reduces acetylation… (more)

Subjects/Keywords: Immunology and Infectious Disease

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

APA (6^th Edition):

Bush, K. (2011). Role for Histone Deacetylases in Glucocorticoid Receptor Mediated Transpression of Natural Killer Cell Activity. (Thesis). Loyola University Chicago. Retrieved from http://ecommons.luc.edu/luc_theses/567

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):

Bush, Kristin. “Role for Histone Deacetylases in Glucocorticoid Receptor Mediated Transpression of Natural Killer Cell Activity.” 2011. Thesis, Loyola University Chicago. Accessed February 25, 2020. http://ecommons.luc.edu/luc_theses/567.

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

MLA Handbook (7^th Edition):

Bush, Kristin. “Role for Histone Deacetylases in Glucocorticoid Receptor Mediated Transpression of Natural Killer Cell Activity.” 2011. Web. 25 Feb 2020.

Vancouver:

Bush K. Role for Histone Deacetylases in Glucocorticoid Receptor Mediated Transpression of Natural Killer Cell Activity. [Internet] [Thesis]. Loyola University Chicago; 2011. [cited 2020 Feb 25]. Available from: http://ecommons.luc.edu/luc_theses/567.

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

Council of Science Editors:

Bush K. Role for Histone Deacetylases in Glucocorticoid Receptor Mediated Transpression of Natural Killer Cell Activity. [Thesis]. Loyola University Chicago; 2011. Available from: http://ecommons.luc.edu/luc_theses/567

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

Loyola University Chicago

10. Hlavin, Sara. Binge Ethanol Leads to Decreased Macrophage Accumulation in Infected Cutaneous Wounds.

Degree: MS, Microbiology and Immunology, 2012, Loyola University Chicago

URL: http://ecommons.luc.edu/luc_theses/720

► Trauma patients who consumed alcohol prior to sustaining injuries have higher rates of morbidity and mortality than those with comparable injuries who did not… (more)

▼ Trauma patients who consumed alcohol prior to sustaining injuries have higher rates of morbidity and mortality than those with comparable injuries who did not drink. Additionally, those who drank had impaired wound healing and increased susceptibility to infection. Despite these clinical observations, few studies have explored the effect of ethanol on the innate immune cell function in a healing wound or how this may alter resolution of cutaneous infection. A murine model of ethanol and cutaneous wound infection was used to examine bacterial growth and recruitment of innate immune cells. Mice were given either ethanol (2.2 g/kg) or saline 30 minutes prior to being subjected to six 3 mm dorsal punch wounds and Staphylococcus aureus (104 CFU/wound). At 24 hours after injury and infection, wound tissue was collected. There was a 3.6 fold increase in bacterial growth in the infected wounds of ethanol-exposed mice relative to those given vehicle prior to wound infection. This elevated bacterial growth was accompanied by an increase in the percentage of open wound area realative to wounds from mice that were immediately sacrificed after being injured (p<0.0001). To determine the contribution of ethanol-related alterations in the innate immune response to this heightened bacterial colonization, we examined wound neutrophil and macrophage accumulation in the wounds by immunofluorescent imaging. At 24 hours, no differences were observed in the number of neutrophils at the infected wound site regardless of ethanol exposure. In contrast, macrophage accumulation was 45% lower in wounds from ethanol-exposed mice relative to vehicle-treated animals (p<0.05). This decrease in macrophage recruitement was accompanied by a 24% reduction in the level of macrophage chemoattractant protein-1 (MCP-1) in wound homogenates from ethanol exposed mice, however, this differences was not significant. Consistent with the lack of change in the number of wound neutrophils, we also failed to detect a difference in the wound content of neutrophil chemokines, KC and macrophage inflammatory protein-2 (MIP-2). To further explore differences in innate immune response due to alcohol, we examined phagocytosis of S. aureus by neutrophils and macrophages in the wound. However, no evidence of phagocytosis by either cell was observed due to a lack of bacterial dissemination into the tissue adjacent to the wound. Together, these data show that ethanol impairs macrophage accumulation at the infected wound site 24 hours after injury and suggest that the reduction in these cells in ethanol-exposed mice could contribute to reduced bacterial clearance and increased wound size.

Subjects/Keywords: Immunology and Infectious Disease

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

APA (6^th Edition):

Hlavin, S. (2012). Binge Ethanol Leads to Decreased Macrophage Accumulation in Infected Cutaneous Wounds. (Thesis). Loyola University Chicago. Retrieved from http://ecommons.luc.edu/luc_theses/720

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):

Hlavin, Sara. “Binge Ethanol Leads to Decreased Macrophage Accumulation in Infected Cutaneous Wounds.” 2012. Thesis, Loyola University Chicago. Accessed February 25, 2020. http://ecommons.luc.edu/luc_theses/720.

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

MLA Handbook (7^th Edition):

Hlavin, Sara. “Binge Ethanol Leads to Decreased Macrophage Accumulation in Infected Cutaneous Wounds.” 2012. Web. 25 Feb 2020.

Vancouver:

Hlavin S. Binge Ethanol Leads to Decreased Macrophage Accumulation in Infected Cutaneous Wounds. [Internet] [Thesis]. Loyola University Chicago; 2012. [cited 2020 Feb 25]. Available from: http://ecommons.luc.edu/luc_theses/720.

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

Council of Science Editors:

Hlavin S. Binge Ethanol Leads to Decreased Macrophage Accumulation in Infected Cutaneous Wounds. [Thesis]. Loyola University Chicago; 2012. Available from: http://ecommons.luc.edu/luc_theses/720

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

Loyola University Chicago

11. Foley, Kendra. Tcr Modifications to Enhance Expression, Chain Pairing, and Antigen Recognition for Adoptive T Cell Transfer.

Degree: MS, Microbiology and Immunology, 2015, Loyola University Chicago

URL: http://ecommons.luc.edu/luc_theses/2784

► T cell receptor (TCR) gene modified T cells for adoptive T cell transfer therapy have been shown to have clinical success in treating melanoma… (more)

Subjects/Keywords: Immunology and Infectious Disease

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APA (6^th Edition):

Foley, K. (2015). Tcr Modifications to Enhance Expression, Chain Pairing, and Antigen Recognition for Adoptive T Cell Transfer. (Thesis). Loyola University Chicago. Retrieved from http://ecommons.luc.edu/luc_theses/2784

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):

Foley, Kendra. “Tcr Modifications to Enhance Expression, Chain Pairing, and Antigen Recognition for Adoptive T Cell Transfer.” 2015. Thesis, Loyola University Chicago. Accessed February 25, 2020. http://ecommons.luc.edu/luc_theses/2784.

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

MLA Handbook (7^th Edition):

Foley, Kendra. “Tcr Modifications to Enhance Expression, Chain Pairing, and Antigen Recognition for Adoptive T Cell Transfer.” 2015. Web. 25 Feb 2020.

Vancouver:

Foley K. Tcr Modifications to Enhance Expression, Chain Pairing, and Antigen Recognition for Adoptive T Cell Transfer. [Internet] [Thesis]. Loyola University Chicago; 2015. [cited 2020 Feb 25]. Available from: http://ecommons.luc.edu/luc_theses/2784.

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

Council of Science Editors:

Foley K. Tcr Modifications to Enhance Expression, Chain Pairing, and Antigen Recognition for Adoptive T Cell Transfer. [Thesis]. Loyola University Chicago; 2015. Available from: http://ecommons.luc.edu/luc_theses/2784

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

Loyola University Chicago

12. Cannon, Abigail Rhea. Role of Heat Shock Proteins in Maintenance of the Gut Barrier Following Burn Injury.

Degree: MS, Microbiology and Immunology, 2015, Loyola University Chicago

URL: http://ecommons.luc.edu/luc_theses/3127

► Introduction: Burn injury remains a prominent clinical problem. Patients suffering from burns often succumb to secondary infectious complications leading to sepsis and widespread tissue… (more)

▼ Introduction: Burn injury remains a prominent clinical problem. Patients suffering from burns often succumb to secondary infectious complications leading to sepsis and widespread tissue injury ending in Multiple Organ Dysfunction. However, the mechanism behind the onset of these extraneous symptoms following burn injury is not fully understood. The integrity of the gut barrier is of critical importance as it harbors the largest bacterial reservoir in the body. Following burn injury, we observed a breakdown of the gut barrier resulting in increased gut leakiness and bacterial translocation. Under homeostatic conditions, heat shock proteins (HSPs) stabilize tight junction proteins. Particularly, HSP72 is shown to play a role in stabilizing tight junctional complexes of the blood brain barrier. Since tight junction proteins are responsible for maintaining gut barrier integrity, we examined the effect of burn injury on the heat shock response via HSPs and the claudin and occludin family of tight junction proteins. Hypothesis: Burn injury suppresses heat shock protein expression, which leads to alterations in tight junction proteins contributing to increased intestinal permeability and bacterial translocation after injury. Methods: Male C57BL/6 (10-12 week old) mice were anesthetized and administered an ~20% total body surface area dorsal scald burn using 85⁰C water for ~7-9 seconds and resuscitated with 1mL normal saline. The small and large intestines were harvested 4 hours, one, and three days following burn injury and processed for isolation of intestinal epithelial cells (IEC). IEC HSP25, 72, and 90 mRNA expression was examined by q-RTPCR along with claudin-4, claudin-8, and occludin. Protein levels of HSP25 and 72 and then claudin-4 and claudin-8 were examined by ELISA and immunofluorescence staining respectively. Results: We found significant decreases in HSP25, 72, and 90 expression (25%, 85%, and 51% respectively) in IECs harvested from the small intestine one day post burn injury compared to sham controls. This accompanied a significant decrease in claudin-4 and -8 expression (54% and 49%) in small intestine IECs of burn animals one day after burn compared to sham controls. At the protein level, burn injury resulted in a decrease of 85% in HSP25 four hours after burn injury and significant decreases in HSP72 four (51%) and three days (46%) in small intestine IECs compared to sham controls. Upon assessment of immunofluorescence staining of TJ proteins one day after burn injury, we observed significant decreases in claudin-4 levels, but claudin-8 immunofluorescence staining is still in progress. To discourage biases, we are currently expanding our immunofluorescence staining of tight junction proteins to include more tissue sections. Analysis of expression HSP25, 72, and 90 in large intestine IECS one day after burn injury resulted in a significant decrease in all three HSPs 4 hours of 44%, 79%, and 33% respectively after injury compared to sham. This significant decrease in HSP72…

Subjects/Keywords: Immunology and Infectious Disease

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

APA (6^th Edition):

Cannon, A. R. (2015). Role of Heat Shock Proteins in Maintenance of the Gut Barrier Following Burn Injury. (Thesis). Loyola University Chicago. Retrieved from http://ecommons.luc.edu/luc_theses/3127

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):

Cannon, Abigail Rhea. “Role of Heat Shock Proteins in Maintenance of the Gut Barrier Following Burn Injury.” 2015. Thesis, Loyola University Chicago. Accessed February 25, 2020. http://ecommons.luc.edu/luc_theses/3127.

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

MLA Handbook (7^th Edition):

Cannon, Abigail Rhea. “Role of Heat Shock Proteins in Maintenance of the Gut Barrier Following Burn Injury.” 2015. Web. 25 Feb 2020.

Vancouver:

Cannon AR. Role of Heat Shock Proteins in Maintenance of the Gut Barrier Following Burn Injury. [Internet] [Thesis]. Loyola University Chicago; 2015. [cited 2020 Feb 25]. Available from: http://ecommons.luc.edu/luc_theses/3127.

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

Council of Science Editors:

Cannon AR. Role of Heat Shock Proteins in Maintenance of the Gut Barrier Following Burn Injury. [Thesis]. Loyola University Chicago; 2015. Available from: http://ecommons.luc.edu/luc_theses/3127

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

13. Uprety, Tirth. Role of Bovine Ileal Sub-epithelial Myofibroblasts and Epithelial Cells in Innate Immunity.

Degree: MS, Biology and Microbiology, 2018, South Dakota State University

URL: https://openprairie.sdstate.edu/etd/2942

► Gastro-intestinal (GI) tract harbors largest number of microbiota as well as the largest number of immune cells for a given tissue. The host needs… (more)

▼ Gastro-intestinal (GI) tract harbors largest number of microbiota as well as the largest number of immune cells for a given tissue. The host needs to mount an effective immune response against invading pathogens and tolerance against commensals. Thus, regulatory mechanism and barrier function of the GI tract are of utmost importance for appropriate host microbe interaction and gut homeostasis. Intestinal epithelial cells (IECs) act as the first line of defense against invading pathogens. IECs recognize pathogens and commensals and mount an effective innate immune response. Such recognition of pathogens is mediated through germ line encoded pattern recognition receptors (PRRs). Intestinal sub-epithelial myofibroblasts (ISEMFs) reside just beneath the surface epithelium and are involved in maturation and differentiation of epithelium. ISEMFs protect from pathogens that breach surface epithelium by expressing PRRs. Lack of stable intestinal epithelial and sub-epithelial myofibroblast cell lines has slowed down scientific studies on these cells. In this study, we established and characterized ISEMF cells from the ileum of a 2-day old calf. We also had generated stable bovine ileal epithelial cell (BIEC-c4) cultures in our lab. On real time-quantitative polymerase chain reaction (RT-qPCR) analysis both these cell types expressed Toll-like receptors (TLRs) 1-9. To investigate their responses to various pathogen-associated molecular patterns (PAMPs), we stimulated both cell types for 3 hours and 24 hours with various PAMPs. The RT-qPCR assay was used to investigate changes in TLR gene expression and in cytokine genes following stimulation. Lipopolysaccharide, peptidoglycan, and flagellin were used as bacterial ligands of surface PRRs. Similarly, γ-D-Glu-mDAP, muramyl dipeptide, polyinosonic:polycytidylic acid, poly I:C complexed with lyovec, and imiquimod were used as ligands of cytosolic and endosomal PRRs. Bovine ileal ISEMFs responded to bacterial PAMPs and to ligands of cytosolic and endosomal PRRs by significantly altering TLR gene expression. Unlike bovine ISEMFs, BIEC-c4 cells responded only to bacterial ligands. Thus, we conclude that bovine ileal ISEMF can be a good model to study innate immune responses and signaling pathways occurring at subepithelial compartment. However, BIEC-c4 cells may serve as a good in-vitro model to study enteric infectious disease pathogenesis and innate immune responses associated with them. Advisors/Committee Members: Radhey Shyam Kaushik.

Subjects/Keywords: Immunology and Infectious Disease; Microbiology

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

APA (6^th Edition):

Uprety, T. (2018). Role of Bovine Ileal Sub-epithelial Myofibroblasts and Epithelial Cells in Innate Immunity. (Masters Thesis). South Dakota State University. Retrieved from https://openprairie.sdstate.edu/etd/2942

Chicago Manual of Style (16^th Edition):

Uprety, Tirth. “Role of Bovine Ileal Sub-epithelial Myofibroblasts and Epithelial Cells in Innate Immunity.” 2018. Masters Thesis, South Dakota State University. Accessed February 25, 2020. https://openprairie.sdstate.edu/etd/2942.

MLA Handbook (7^th Edition):

Uprety, Tirth. “Role of Bovine Ileal Sub-epithelial Myofibroblasts and Epithelial Cells in Innate Immunity.” 2018. Web. 25 Feb 2020.

Vancouver:

Uprety T. Role of Bovine Ileal Sub-epithelial Myofibroblasts and Epithelial Cells in Innate Immunity. [Internet] [Masters thesis]. South Dakota State University; 2018. [cited 2020 Feb 25]. Available from: https://openprairie.sdstate.edu/etd/2942.

Council of Science Editors:

Uprety T. Role of Bovine Ileal Sub-epithelial Myofibroblasts and Epithelial Cells in Innate Immunity. [Masters Thesis]. South Dakota State University; 2018. Available from: https://openprairie.sdstate.edu/etd/2942

Loyola University Chicago

14. Keller, Taylor. Cell Intrinsic Characteristics of Cord Blood Naive CD4 T Cells.

Degree: MS, Microbiology and Immunology, 2018, Loyola University Chicago

URL: https://ecommons.luc.edu/luc_theses/3682

► The neonatal immune system is functionally distinct from the adult immune system. Neonatal immune responses are less reactive than their adult counterparts, and as… (more)

Subjects/Keywords: Immunology and Infectious Disease

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APA (6^th Edition):

Keller, T. (2018). Cell Intrinsic Characteristics of Cord Blood Naive CD4 T Cells. (Thesis). Loyola University Chicago. Retrieved from https://ecommons.luc.edu/luc_theses/3682

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):

Keller, Taylor. “Cell Intrinsic Characteristics of Cord Blood Naive CD4 T Cells.” 2018. Thesis, Loyola University Chicago. Accessed February 25, 2020. https://ecommons.luc.edu/luc_theses/3682.

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

MLA Handbook (7^th Edition):

Keller, Taylor. “Cell Intrinsic Characteristics of Cord Blood Naive CD4 T Cells.” 2018. Web. 25 Feb 2020.

Vancouver:

Keller T. Cell Intrinsic Characteristics of Cord Blood Naive CD4 T Cells. [Internet] [Thesis]. Loyola University Chicago; 2018. [cited 2020 Feb 25]. Available from: https://ecommons.luc.edu/luc_theses/3682.

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

Council of Science Editors:

Keller T. Cell Intrinsic Characteristics of Cord Blood Naive CD4 T Cells. [Thesis]. Loyola University Chicago; 2018. Available from: https://ecommons.luc.edu/luc_theses/3682

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

University of Louisville

15. Armstrong, Cortney Linn. Characterization of Filifactor alocis and its immune evasion strategies employed against human neutrophils.

Degree: PhD, 2017, University of Louisville

URL: 10.18297/etd/2769 ; https://ir.library.louisville.edu/etd/2769

► Periodontal disease is among the most common of inflammatory conditions and is caused by bacterial and host derived factors. The presence of bacteria drives… (more)

▼ Periodontal disease is among the most common of inflammatory conditions and is caused by bacterial and host derived factors. The presence of bacteria drives the recruitment of neutrophils, professional phagocytes, to migrate to specific oral sites where they produce potent antimicrobials to kill their target. However, this inflammation and production of antimicrobials must be strictly regulated to minimize collateral host tissue damage. Human neutrophils recognized the oral pathogen Filifactor alocis through Toll-like receptor (TLR) 2 and upon binding, activated both p38 MAPK and ERK signaling pathways, known to be involved in neutrophil cell migration and degranulation. F. alocis also stimulated secretory vesicle and specific granule exocytosis and enhanced chemokinetic and chemotactic migration to interleukin (IL)-8, a key chemoattractant found in the oral cavity (Chapter 2). Once these challenged neutrophils have arrived at their targeted site, they will employ oxidative-mediated killing mechanisms, operating intracellularly in the bacterial-containing phagosome, and extracellularly, in the extracellular space. Neutrophils effectively perform phagocytosis to internalize F. alocis into their phagosomal compartment, however minimal intracellular respiratory burst response is produced. In addition, F. alocis-challenged neutrophils produced minimal superoxide release, however the bacterial challenge primed neutrophils for an enhanced respiratory burst response. F. alocis survived neutrophil oxygen-dependent intracellular and extracellular killing mechanisms up to 4 h post-infection (Chapter 3). Activated neutrophils can also undergo neutrophil extracellular trap (NET) formation as a means to trap and potentially kill targets. NETs have been described to be formed in the oral cavity in response to oral biofilms. F. alocis failed to induce NETs from neutrophils, which may indicate this bacterium is unique to the oral cavity, as other oral bacteria Streptococcus gordonii and Peptoanaerobacter stomatis induce NETs. However, F. alocis can manipulate neutrophils and reduce their NET formation capacities to known pharmacological (PMA) and bacterial (S. gordonii) inducers (Chapter 4). Overall, our results are the first to show how F. alocis effectively evades human neutrophil killing mechanisms and manipulates some of their functional responses. These results provide information about the pathogenic potential of F. alocis which would help delineate the role of this emerging pathogen in the development of periodontal disease. Advisors/Committee Members: Uriarte, Silvia M., Alard, Pascale, Lamont, Richard J., Miller, Richard D., Graham, James E..

Subjects/Keywords: Immunology of Infectious Disease

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

APA (6^th Edition):

Armstrong, C. L. (2017). Characterization of Filifactor alocis and its immune evasion strategies employed against human neutrophils. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/2769 ; https://ir.library.louisville.edu/etd/2769

Chicago Manual of Style (16^th Edition):

Armstrong, Cortney Linn. “Characterization of Filifactor alocis and its immune evasion strategies employed against human neutrophils.” 2017. Doctoral Dissertation, University of Louisville. Accessed February 25, 2020. 10.18297/etd/2769 ; https://ir.library.louisville.edu/etd/2769.

MLA Handbook (7^th Edition):

Armstrong, Cortney Linn. “Characterization of Filifactor alocis and its immune evasion strategies employed against human neutrophils.” 2017. Web. 25 Feb 2020.

Vancouver:

Armstrong CL. Characterization of Filifactor alocis and its immune evasion strategies employed against human neutrophils. [Internet] [Doctoral dissertation]. University of Louisville; 2017. [cited 2020 Feb 25]. Available from: 10.18297/etd/2769 ; https://ir.library.louisville.edu/etd/2769.

Council of Science Editors:

Armstrong CL. Characterization of Filifactor alocis and its immune evasion strategies employed against human neutrophils. [Doctoral Dissertation]. University of Louisville; 2017. Available from: 10.18297/etd/2769 ; https://ir.library.louisville.edu/etd/2769

Wayne State University

16. Gibson, Heather. Ctla-4 transcriptional activation: regulation of induced expression.

Degree: PhD, Immunology and Microbiology, 2011, Wayne State University

URL: https://digitalcommons.wayne.edu/oa_dissertations/237

► Cytotoxic T-lymphocyte antigen 4 (CTLA-4) is a T cell surface protein that is homologous to CD28 and binds to the B7 family of ligands.… (more)

▼ Cytotoxic T-lymphocyte antigen 4 (CTLA-4) is a T cell surface protein that is homologous to CD28 and binds to the B7 family of ligands. Unlike CD28, CTLA-4 interaction transmits a negative signal in T cells, leading to suppression of proliferation. CTLA-4 is constitutively expressed on regulatory T cells (Tregs) but is also inducible in effector T cells. The mechanisms driving transcriptional regulation of CTLA-4 are poorly understood. Our previous work identified a bona fide NFAT1 binding site in the proximal promoter for effector T cells. In addition, we found histone acetylation occurred after stimulation. As a result of its role in suppressing T cell proliferation, CTLA-4 is important for regulation of T cell responses. CTLA-4-immunoglobulin fusion proteins have shown efficacy to quell the overactive immune system in various types of autoimmune diseases. Alternatively, blocking antibodies to CTLA-4 have been used in cancer therapies to boost the anti-tumor immune response. Malignant cells of cutaneous T cell lymphoma (CTCL) express elevated levels of CTLA-4, which may contribute to reduced tumor immunity as the disease progresses. The objective of this work was to identify mechanisms of transcriptional regulation of CTLA-4 to better understand how this gene can be modulated to potentially cater the immune response for a variety of immune-mediated diseases. The major findings of this work include a mechanism by which proteasome inhibition augments CTLA-4 transcription in normal primary human CD4 T cells. The Th2 associated transcription factor GATA3 is both elevated and activated by phosphorylation after treatment with the proteasome inhibitor bortezomib, which in turn leads to CTLA-4 transcriptional activation in primary CD4 T cells. This finding may in part explain the increase in CTLA-4 found in CTCL, where GATA3 is also more abundant, particularly in its phosphorylated state. The increased CTLA-4 in our primary cell model is capable of suppressing T cell proliferation, demonstrating the potency of transcriptional modulation of this gene. Additionally we explored epigenetic and topological modifications that occur for CTLA-4 activation. We found the histone acetyltransferases p300 is responsible for histone 3 acetylation at the CTLA-4 promoter, and its activity is required for CTLA-4 transcription. We also discovered a previously undiscovered role for topoisomerase I in expression of a variety of induced genes, including CTLA-4. These results define novel mechanisms governing transcriptional activation of CTLA-4 in human effector CD4 T cells. Advisors/Committee Members: Henry K. Wong, Wei-Zen Wei.

Subjects/Keywords: Immunology and Infectious Disease

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

APA (6^th Edition):

Gibson, H. (2011). Ctla-4 transcriptional activation: regulation of induced expression. (Doctoral Dissertation). Wayne State University. Retrieved from https://digitalcommons.wayne.edu/oa_dissertations/237

Chicago Manual of Style (16^th Edition):

Gibson, Heather. “Ctla-4 transcriptional activation: regulation of induced expression.” 2011. Doctoral Dissertation, Wayne State University. Accessed February 25, 2020. https://digitalcommons.wayne.edu/oa_dissertations/237.

MLA Handbook (7^th Edition):

Gibson, Heather. “Ctla-4 transcriptional activation: regulation of induced expression.” 2011. Web. 25 Feb 2020.

Vancouver:

Gibson H. Ctla-4 transcriptional activation: regulation of induced expression. [Internet] [Doctoral dissertation]. Wayne State University; 2011. [cited 2020 Feb 25]. Available from: https://digitalcommons.wayne.edu/oa_dissertations/237.

Council of Science Editors:

Gibson H. Ctla-4 transcriptional activation: regulation of induced expression. [Doctoral Dissertation]. Wayne State University; 2011. Available from: https://digitalcommons.wayne.edu/oa_dissertations/237

Wayne State University

17. Rao, Pushpa Durgesh. Alterations In Ocular Surface System During The Pathogenesis Of Herpes Stromal Keratitis.

Degree: PhD, Anatomy and Cell Biology, 2019, Wayne State University

URL: https://digitalcommons.wayne.edu/oa_dissertations/2181

► Herpes stromal keratitis (HSK) is a chronic immuno-inflammatory ocular disease caused by Herpes simplex virus-1 (HSV-1) infection in the cornea. HSK is characterized by… (more)

▼ Herpes stromal keratitis (HSK) is a chronic immuno-inflammatory ocular disease caused by Herpes simplex virus-1 (HSV-1) infection in the cornea. HSK is characterized by the development of corneal opacity and angiogenesis accompanied by the loss of corneal transparency. Despite extensive studies on inhibiting corneal angiogenesis and strategies to reduce HSK disease development, a key underlying mechanism to maintain an intact and a transparent corneal surface during HSK disease progression, remain obscure. Our study has addressed possible causes for the HSK disease severity by identifying the key factors such as the development of inflammatory hypoxia, reduced tear volume, Inflammation of extra-orbital lacrimal gland and the conjunctiva and the transdifferentiation of the corneal epithelium in the HSK developing eyes. Intriguingly, our study also emphasizes the protective role of IGFBP-3 in inhibiting the severe disease progression of HSK. During the pre-clinical and the clinical disease phase of HSK, the influx of neutrophils have been studied as the most prominent innate immune cell type. Development of corneal hem- and lymph-angiogenesis, opacity and epithelial defects hinders the clear vision and is known to be the cause of the increased neutrophil influx in HSV-1 infected cornea. Previous studies have indicated that the influx of neutrophils into mucosal tissue can re-model the development of inflammatory hypoxia. Therefore, the aim of this study was to investigate the development of hypoxia and hypoxia-associated gene expression during the progression of HSK disease. Our results showed an increased influx of neutrophils during the clinical disease of HSK that leads to the development of hypoxia, and the upregulation of hypoxia-associated genes. This study provided us novel insights on the prevalence of the glycolytic metabolism in the HSK developing eyes. Additionally, our data demonstrated that the blocking of Hypoxia-Inducible Factor (HIF) with Acriflavine alone might not be an efficacious drug in reducing HSK disease severity. Overall, these results pave way for using novel therapeutic targets that play a dual role to block HIF and control corneal inflammation during HSK. Maintaining a healthy corneal epithelium, retaining a steady tear volume and its secretion could be the other factors that may aid in alleviating HSK disease severity. Mounting evidence corroborates corneal nerves as a critical factor in the maintenance of corneal integrity and homeostasis of the ocular surface by mediating the reflex actions of blinking and tearing. In support, in a mouse model during HSV-1 ocular infection, corneal nerve damage has been demonstrated. Hence, corneal transparency and clear vision are critically dependent upon the integrity of corneal tissue maintained by the intricate network of corneal nerves, the presence of intact corneal epithelium and tear film that is controlled by a cross-talk between the components of the lacrimal functional unit. Our study showed a reduced… Advisors/Committee Members: Susmit Suvas.

Subjects/Keywords: Immunology and Infectious Disease

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

APA (6^th Edition):

Rao, P. D. (2019). Alterations In Ocular Surface System During The Pathogenesis Of Herpes Stromal Keratitis. (Doctoral Dissertation). Wayne State University. Retrieved from https://digitalcommons.wayne.edu/oa_dissertations/2181

Chicago Manual of Style (16^th Edition):

Rao, Pushpa Durgesh. “Alterations In Ocular Surface System During The Pathogenesis Of Herpes Stromal Keratitis.” 2019. Doctoral Dissertation, Wayne State University. Accessed February 25, 2020. https://digitalcommons.wayne.edu/oa_dissertations/2181.

MLA Handbook (7^th Edition):

Rao, Pushpa Durgesh. “Alterations In Ocular Surface System During The Pathogenesis Of Herpes Stromal Keratitis.” 2019. Web. 25 Feb 2020.

Vancouver:

Rao PD. Alterations In Ocular Surface System During The Pathogenesis Of Herpes Stromal Keratitis. [Internet] [Doctoral dissertation]. Wayne State University; 2019. [cited 2020 Feb 25]. Available from: https://digitalcommons.wayne.edu/oa_dissertations/2181.

Council of Science Editors:

Rao PD. Alterations In Ocular Surface System During The Pathogenesis Of Herpes Stromal Keratitis. [Doctoral Dissertation]. Wayne State University; 2019. Available from: https://digitalcommons.wayne.edu/oa_dissertations/2181

University of Iowa

18. Lifton, Samuel Robert. Retroviral mutagenesis in a newly developed myc transgenic mouse model of human B cell and plasma cell neoplasia.

Degree: MS, Interdisciplinary Studies in Immunology, 2013, University of Iowa

URL: https://ir.uiowa.edu/etd/1479

► Three potential driver genes were identified by use of retroviral mutagenesis in the newly developed iMyc model of B cell malignancy. To do so,… (more)

Subjects/Keywords: Immunology of Infectious Disease

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APA (6^th Edition):

Lifton, S. R. (2013). Retroviral mutagenesis in a newly developed myc transgenic mouse model of human B cell and plasma cell neoplasia. (Masters Thesis). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/1479

Chicago Manual of Style (16^th Edition):

Lifton, Samuel Robert. “Retroviral mutagenesis in a newly developed myc transgenic mouse model of human B cell and plasma cell neoplasia.” 2013. Masters Thesis, University of Iowa. Accessed February 25, 2020. https://ir.uiowa.edu/etd/1479.

MLA Handbook (7^th Edition):

Lifton, Samuel Robert. “Retroviral mutagenesis in a newly developed myc transgenic mouse model of human B cell and plasma cell neoplasia.” 2013. Web. 25 Feb 2020.

Vancouver:

Lifton SR. Retroviral mutagenesis in a newly developed myc transgenic mouse model of human B cell and plasma cell neoplasia. [Internet] [Masters thesis]. University of Iowa; 2013. [cited 2020 Feb 25]. Available from: https://ir.uiowa.edu/etd/1479.

Council of Science Editors:

Lifton SR. Retroviral mutagenesis in a newly developed myc transgenic mouse model of human B cell and plasma cell neoplasia. [Masters Thesis]. University of Iowa; 2013. Available from: https://ir.uiowa.edu/etd/1479

University of Iowa

19. Parlet, Corey Patrick. Mechanisms by which chronic ethanol consumption impairs cutaneous immunity.

Degree: PhD, Immunology, 2014, University of Iowa

URL: https://ir.uiowa.edu/etd/4712

► The immunosuppressive effects of chronic alcohol abuse are profound, wide-ranging and readily apparent at the body's barriers. In the skin, alcoholism is associated with… (more)

▼ The immunosuppressive effects of chronic alcohol abuse are profound, wide-ranging and readily apparent at the body's barriers. In the skin, alcoholism is associated with an increased incidence and severity of infection; yet the precise immunologic alterations responsible remain poorly understood. Cutaneous homeostasis and immunity are afforded via coordinated efforts of tissue-specific immune cell networks. Here, the Meadows-Cook murine model of alcoholism was used to investigate the impact of chronic ethanol (EtOH) exposure upon the following: 1) the composition and function of skin-resident dendritic cells (DCs) and T cells in preimmune mice 2) infection outcome and host defense following Staphylococcus aureus skin infection 3) the induction of cutaneous oxidative stress Chronic EtOH feeding caused a baseline reduction in skin DCs and T cells with the most pronounced effects occurring in self-renewing compartments (i.e, Langerhans cells and γδ T cells). In addition, we found that EtOH-induced immune cell subset loss was often associated with dysfunction of the remaining population. For DCs, EtOH-induced hyporesponsiveness was observed in both in vitro and in vivo migration assays. Defects in the former system could be corrected via TNFα restoration. EtOH-induced dysfunction in skin T cells was evident by the decreased upregulation of JAML and diminished production of IL-17 by epidermal and dermal γδ T cells respectively. In a murine model of EtOH withdrawal, some but not all of the EtOH-induced defects occurring in skin DCs and T cells recovered after cessation of EtOH exposure. Prior to this work, the impact of chronic EtOH exposure upon the cutaneous immune system had not been investigated in a murine model of infection. Using a novel method of cutaneous S. aureus challenge, evidence of exacerbated staphylococcal disease in EtOH-fed mice included skin lesions that were larger and contained more organisms, greater weight loss and increased bacterial dissemination. Infected EtOH-fed mice demonstrated poor maintenance and induction of PMN responses in the skin and draining LNs respectively. Additionally, altered PMN dynamics in the skin of these mice corresponded with reduced production of IL-23 and IL-1β by CD11b+ myeloid cells and IL-17 production by γδ T cells, with the latter defect occurring in the draining LNs as well. In addition, IL-17 restoration via intradermal injection improved bacterial clearance defects in EtOH-fed mice. Taken together, these findings show that the EtOH-induced increase in S. aureus-related injury/illness (i.e., weight loss, bacterial burden, lesion size) corresponds with defects in the IL-23/IL-17 inflammatory axis and poor PMN accumulation at the site of infection and draining LNs. Finally, two complementary tools (mice deficient in molecules that promote or inhibit reactive oxygen species induction) were used to investigate the role of oxidative stress as a driver of cutaneous immune dysfunction. In these studies intriguing evidence was obtained indicating… Advisors/Committee Members: Schlueter, Annette J. (supervisor).

Subjects/Keywords: Immunology of Infectious Disease

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APA (6^th Edition):

Parlet, C. P. (2014). Mechanisms by which chronic ethanol consumption impairs cutaneous immunity. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/4712

Chicago Manual of Style (16^th Edition):

Parlet, Corey Patrick. “Mechanisms by which chronic ethanol consumption impairs cutaneous immunity.” 2014. Doctoral Dissertation, University of Iowa. Accessed February 25, 2020. https://ir.uiowa.edu/etd/4712.

MLA Handbook (7^th Edition):

Parlet, Corey Patrick. “Mechanisms by which chronic ethanol consumption impairs cutaneous immunity.” 2014. Web. 25 Feb 2020.

Vancouver:

Parlet CP. Mechanisms by which chronic ethanol consumption impairs cutaneous immunity. [Internet] [Doctoral dissertation]. University of Iowa; 2014. [cited 2020 Feb 25]. Available from: https://ir.uiowa.edu/etd/4712.

Council of Science Editors:

Parlet CP. Mechanisms by which chronic ethanol consumption impairs cutaneous immunity. [Doctoral Dissertation]. University of Iowa; 2014. Available from: https://ir.uiowa.edu/etd/4712

University of Iowa

20. Vacaflores Salinas, Aldo Fabian. New roles for an old cytokine : characterizing how exposure to Il-12 alters human CD4 And CD8 T cell responses.

Degree: PhD, Immunology, 2016, University of Iowa

URL: https://ir.uiowa.edu/etd/2157

► CD4 and CD8 T cells are constantly exposed to inflammatory signals that influence diverse functional outcomes during infections and certain autoimmune disorders. One of… (more)

▼ CD4 and CD8 T cells are constantly exposed to inflammatory signals that influence diverse functional outcomes during infections and certain autoimmune disorders. One of the signals controlling CD4 and CD8 T cell functions is the inflammatory cytokine IL-12. Previous studies have focused on how IL-12 regulates CD4 and CD8 T cell functions when present during or after the activation of the T cell receptor (TCR). However, based on murine studies, we have only recently begun to appreciate that exposure to inflammatory signals, driven in part by IL-12, could alter how CD4 and CD8 T cells respond to TCR stimulation. Although intriguing, these studies have left several questions unanswered. Does IL-12 similarly regulate the function of human T cells? If so, what is the exact molecular mechanism by which IL-12 mediates these effects? To address these critical questions, we examined how IL-12 pretreatment altered human CD4 and CD8 T cell responses to subsequent TCR stimulation. In CHAPTER III, we examined how prior exposure to IL-12 alters the responses of human CD4 T cells to subsequent TCR stimulation. Some of our key findings were that IL-12 pretreatment increased the production of IFN-γ, TNF-α, IL-13, IL-4 and IL-10 after TCR stimulation, suggesting that prior exposure to IL-12 potentiates the TCR-induced release of a range of cytokines. Based on the intracellular staining and mRNA expression data, we concluded that the IL-12-mediated increased production of a range of cytokines was a consequence of at least two separate mechanisms, increased mRNA expression for IFN-γ and increased release of TNF-α, IL-13, IL-4 and IL-10. In CHAPTER IV, we explored the mechanisms by which IL-12 pretreatment altered human CD4 T cell responses to TCR stimulation. We observed that IL-12 pretreatment increased the phosphorylation of AKT, P38 and LCK following TCR stimulation without altering other TCR signaling molecules, suggesting that this potentially mediates the increase in transcription of cytokines. In addition, the IL-12-mediated enhancement of cytokines that were not transcriptionally regulated was partially driven by increased oxidative metabolism. Collectively our results uncovered a novel function of IL-12 in regulating human CD4 T cell responses; specifically, it enhanced the release of a range of cytokines potentially by altering TCR signaling pathways and by enhancing oxidative metabolism. Then, in CHAPTER V, we examined the effects of IL-12 pretreatment in altering the responses of human CD8 T cells to subsequent TCR stimulation. Our key finding was that pretreatment of human CD8 T cells with IL-12 resulted in increased IFN-γ… Advisors/Committee Members: Houtman, Jon C. D. (supervisor).

Subjects/Keywords: Immunology of Infectious Disease

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APA (6^th Edition):

Vacaflores Salinas, A. F. (2016). New roles for an old cytokine : characterizing how exposure to Il-12 alters human CD4 And CD8 T cell responses. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/2157

Chicago Manual of Style (16^th Edition):

Vacaflores Salinas, Aldo Fabian. “New roles for an old cytokine : characterizing how exposure to Il-12 alters human CD4 And CD8 T cell responses.” 2016. Doctoral Dissertation, University of Iowa. Accessed February 25, 2020. https://ir.uiowa.edu/etd/2157.

MLA Handbook (7^th Edition):

Vacaflores Salinas, Aldo Fabian. “New roles for an old cytokine : characterizing how exposure to Il-12 alters human CD4 And CD8 T cell responses.” 2016. Web. 25 Feb 2020.

Vancouver:

Vacaflores Salinas AF. New roles for an old cytokine : characterizing how exposure to Il-12 alters human CD4 And CD8 T cell responses. [Internet] [Doctoral dissertation]. University of Iowa; 2016. [cited 2020 Feb 25]. Available from: https://ir.uiowa.edu/etd/2157.

Council of Science Editors:

Vacaflores Salinas AF. New roles for an old cytokine : characterizing how exposure to Il-12 alters human CD4 And CD8 T cell responses. [Doctoral Dissertation]. University of Iowa; 2016. Available from: https://ir.uiowa.edu/etd/2157

University of Iowa

21. Rosean, Timothy Robert. The tumor microenvironment is critical for the development of plasma cell neoplasia in mice.

Degree: PhD, Immunology, 2014, University of Iowa

URL: https://ir.uiowa.edu/etd/1497

► Plasma cell neoplasms (PCN), including multiple myeloma, are tumors of terminally differentiated B cells. Despite a significant research effort, and numerous advances in therapy,… (more)

▼ Plasma cell neoplasms (PCN), including multiple myeloma, are tumors of terminally differentiated B cells. Despite a significant research effort, and numerous advances in therapy, most tumors of this B cell lineage remain incurable. To this end, understanding factors which are critical for the development of PCN may lead to new avenues for therapy. Interleukin-6 (IL-6) is a pleiotropic, pro-inflammatory cytokine which supports the growth, proliferation, and survival of myeloma cells. We found that inflammation, and in particular, IL-6 is critical for the development of PCN. In order to determine if tumor microenvironment (TME) or B cell-derived IL-6 was more important in PCN development, we utilized an adoptive transfer system of tumor formation. By adoptively transferring premalignant B cells into recipients, and then providing the B cells with an inflammatory microenvironment through the use of pristane, we were able to generate donor tumors in recipient mice. Utilizing this method, a series of adoptive transfers were performed to determine the primary source of IL-6 in murine PCN development. We discovered that TME-derived IL-6, and not B cell-derived IL-6, is most critical for PCN development. Furthermore, in studying the lesions in B cell development which lead to tumor formation, we discovered that IL-6 collaborates with the proto-oncogene c-Myc in spontaneous germinal center (GC) formation. The spontaneous GCs were accompanied by a robust follicular T helper cell response. In characterizing the genetic lesions which lead to the GC formation, we discovered that Myc-transgenic mice develop a significant increase in the population of B1a B cells. Furthermore, these B1a B cells infiltrate the spontaneous GCs of double transgenic Myc/IL-6 mice. Lastly, utilizing our adoptive transfer method, we determined that the germinal center response is necessary for the development of PCN in mice. Lastly, we focused our efforts on another oncogene which collaborates with IL-6, BCL-2. Double transgenic BCL-2/IL-6 mice develop PCN and spontaneous GCs. Of interest however, the adoptive transfer of BCL-2/IL-6 B cells results in tumor formation without the use of pristane. Furthermore, the adoptive transfer recipients develop bone lesions, hind limb paralysis, and a monoclonal gammopathy. This model closely recapitulates many of the pathophysiological features seen in human PCN. This new model promises to be important for future studies into PCN development and treatment. Advisors/Committee Members: Janz, Siegfried (supervisor).

Subjects/Keywords: publicabstract; Immunology of Infectious Disease

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APA (6^th Edition):

Rosean, T. R. (2014). The tumor microenvironment is critical for the development of plasma cell neoplasia in mice. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/1497

Chicago Manual of Style (16^th Edition):

Rosean, Timothy Robert. “The tumor microenvironment is critical for the development of plasma cell neoplasia in mice.” 2014. Doctoral Dissertation, University of Iowa. Accessed February 25, 2020. https://ir.uiowa.edu/etd/1497.

MLA Handbook (7^th Edition):

Rosean, Timothy Robert. “The tumor microenvironment is critical for the development of plasma cell neoplasia in mice.” 2014. Web. 25 Feb 2020.

Vancouver:

Rosean TR. The tumor microenvironment is critical for the development of plasma cell neoplasia in mice. [Internet] [Doctoral dissertation]. University of Iowa; 2014. [cited 2020 Feb 25]. Available from: https://ir.uiowa.edu/etd/1497.

Council of Science Editors:

Rosean TR. The tumor microenvironment is critical for the development of plasma cell neoplasia in mice. [Doctoral Dissertation]. University of Iowa; 2014. Available from: https://ir.uiowa.edu/etd/1497

University of Iowa

22. Scorza, Breanna M. Interaction of human keratinocytes with Leishmania spp.: a comparative study of Leishmania infantum and Leishmania major.

Degree: PhD, Immunology, 2017, University of Iowa

URL: https://ir.uiowa.edu/etd/5847

► Leishmaniasis refers to the group of diseases caused by pathogenic protozoan parasites of the genus Leishmania. Nearly all human Leishmania spp. infections are initiated… (more)

▼ Leishmaniasis refers to the group of diseases caused by pathogenic protozoan parasites of the genus Leishmania. Nearly all human Leishmania spp. infections are initiated in mammalian skin through the bite of the phlebotomine sand fly vector. However, clinical manifestations vary greatly with infecting species. Leishmania major establish infection locally within the skin and cause chronic ulcerating skin lesions at the local cutaneous site of inoculation, in a syndrome known as Cutaneous Leishmaniasis (CL) Leishmania infantum parasites metastasize from the site of skin infection via unknown mechanisms, and establish infection within visceral organs usually without inducing skin pathology, resulting in the potentially fatal disseminated disease, Visceral Leishmaniasis (VL). Mouse studies suggest early responses at the skin infection site are critical determinants of subsequent adaptive immune responses in leishmaniasis, yet few studies address the role of keratinocytes, the most abundant immunoactive cell in the epidermis. We hypothesize that Leishmania infection causes keratinocytes to produce immunomodulatory factors that influence the outcome of infection. Incubation of primary or immortalized human keratinocytes with L. infantum or L. major elicited dramatically different responses. Keratinocytes incubated with L. infantum significantly increased expression of pro-inflammatory genes IL6, IL8, TNF, and IL1B by RT-qPCR; whereas keratinocytes exposed to L. major did not. Similar to live parasites, L. infantum-derived exosomes induced more IL8 mRNA compared to control or L. major-derived exosomes. Western blotting confirmed NFkBp65 phosphorylation in keratinocytes exposed to L. infantum but not L. major. However, no evidence of L. major inhibition of TNF-induced NFkBp65 phosphorylation was observed in simultaneously treated keratinocytes. To examine whether keratinocytes influence proximal host cells, L. infantum-infected human monocytes were co-cultured with keratinocytes across a transwell membrane. These studies suggested L. infantum-exposed keratinocytes release soluble factors that enhance monocyte control of intracellular L. infantum replication. L. major-exposed keratinocytes had no comparable effect. These data suggest L. infantum and L. major differentially activate keratinocytes to release factors that limit infection in monocytes. Microarray analyses performed on human keratinocytes exposed to either L. infantum or L. major promastigotes identified a limited number of transcripts increased by parasite exposure. Consistent with RT-qPCR observations, several inflammatory cytokine and chemokine genes were more strongly induced in L. infantum-exposed keratinocytes compared to L. major-exposed keratinocytes. Pathway analyses of genes induced by L. infantum-treated keratinocytes suggested that this interaction may induce neutrophil recruitment. Notably, AP1 transcription factor subunit genes were significantly down regulated in L. major-treated compared with L. infantum-treated or… Advisors/Committee Members: Wilson, Mary E. (supervisor).

Subjects/Keywords: Immunology of Infectious Disease

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APA (6^th Edition):

Scorza, B. M. (2017). Interaction of human keratinocytes with Leishmania spp.: a comparative study of Leishmania infantum and Leishmania major. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/5847

Chicago Manual of Style (16^th Edition):

Scorza, Breanna M. “Interaction of human keratinocytes with Leishmania spp.: a comparative study of Leishmania infantum and Leishmania major.” 2017. Doctoral Dissertation, University of Iowa. Accessed February 25, 2020. https://ir.uiowa.edu/etd/5847.

MLA Handbook (7^th Edition):

Scorza, Breanna M. “Interaction of human keratinocytes with Leishmania spp.: a comparative study of Leishmania infantum and Leishmania major.” 2017. Web. 25 Feb 2020.

Vancouver:

Scorza BM. Interaction of human keratinocytes with Leishmania spp.: a comparative study of Leishmania infantum and Leishmania major. [Internet] [Doctoral dissertation]. University of Iowa; 2017. [cited 2020 Feb 25]. Available from: https://ir.uiowa.edu/etd/5847.

Council of Science Editors:

Scorza BM. Interaction of human keratinocytes with Leishmania spp.: a comparative study of Leishmania infantum and Leishmania major. [Doctoral Dissertation]. University of Iowa; 2017. Available from: https://ir.uiowa.edu/etd/5847

University of Iowa

23. Gorman, Jacob. Regulation of T cell responses by the surface receptor Tim-3.

Degree: PhD, Immunology, 2014, University of Iowa

URL: https://ir.uiowa.edu/etd/1326

► Tim-3 (for T cell immunoglobulin and mucin domain 3) is a surface molecule expressed throughout the immune system that appears to mediate both stimulatory… (more)

▼ Tim-3 (for T cell immunoglobulin and mucin domain 3) is a surface molecule expressed throughout the immune system that appears to mediate both stimulatory and inhibitory effects. Tim-3 is expressed by activated CD4 and CD8 T cells, which suggests a direct role in the regulation of T cell responses. Consistent with this possibility, previous studies have shown that blockade of interactions between Tim-3 and ligands in the context of mouse models for autoimmunity and chronic infection can augment T cell responses, which indicates that Tim-3 functions as an inhibitory receptor for T cells. However, other studies have provided evidence that Tim-3 can function to promote T cell responses, which suggests that Tim-3 acts as a stimulatory receptor. In addition, biochemical and cell culture studies have shown that Tim-3 can induce both inhibitory and stimulatory signaling pathways. These conflicting findings highlight that the role of Tim-3 in regulating T cell responses remains unclear and warrants further investigation. My studies sought to determine the role of Tim-3 in regulating T cell responses to microbial infections in vivo and to acute stimulation in vitro. Using Tim-3 KO mice and Tim-3 KO cells, I demonstrate that Tim-3 can directly enhance CD8 T cell responses to Listeria monocytogenes (LM). I also provide evidence that Tim-3 indirectly regulates CD4 T cell responses to LM. Alternatively, I show that Tim-3 may inhibit CD4 and CD8 T cell responses to the chronic viral infection LCMV-Clone 13, and that Tim-3 may be dispensable for T cell responses to the acute viral infection LCMV-Armstrong. Additionally, I demonstrate that Tim-3 expression in response to acute stimulation in vitro or in vivo marks populations of CD4 Th1 cells that are enriched for cells with effector function as measured by cytokine production and markers for degranulation. Collectively, these data suggest that Tim-3 may differentially regulate T cell effector function in a manner that is dependent on infectious environment encountered. Advisors/Committee Members: Colgan, John D. (supervisor).

Subjects/Keywords: Immunology of Infectious Disease

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APA (6^th Edition):

Gorman, J. (2014). Regulation of T cell responses by the surface receptor Tim-3. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/1326

Chicago Manual of Style (16^th Edition):

Gorman, Jacob. “Regulation of T cell responses by the surface receptor Tim-3.” 2014. Doctoral Dissertation, University of Iowa. Accessed February 25, 2020. https://ir.uiowa.edu/etd/1326.

MLA Handbook (7^th Edition):

Gorman, Jacob. “Regulation of T cell responses by the surface receptor Tim-3.” 2014. Web. 25 Feb 2020.

Vancouver:

Gorman J. Regulation of T cell responses by the surface receptor Tim-3. [Internet] [Doctoral dissertation]. University of Iowa; 2014. [cited 2020 Feb 25]. Available from: https://ir.uiowa.edu/etd/1326.

Council of Science Editors:

Gorman J. Regulation of T cell responses by the surface receptor Tim-3. [Doctoral Dissertation]. University of Iowa; 2014. Available from: https://ir.uiowa.edu/etd/1326

University of Iowa

24. Janowski, Ann M. The protective roles of NLRs during infection and tumor progression.

Degree: PhD, Immunology, 2016, University of Iowa

URL: https://ir.uiowa.edu/etd/5518

► The immune system has evolved to fight off numerous pathogens. The first line of defense against these pathogens are innate immune cells. Innate immune… (more)

Subjects/Keywords: Immunology of Infectious Disease

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APA (6^th Edition):

Janowski, A. M. (2016). The protective roles of NLRs during infection and tumor progression. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/5518

Chicago Manual of Style (16^th Edition):

Janowski, Ann M. “The protective roles of NLRs during infection and tumor progression.” 2016. Doctoral Dissertation, University of Iowa. Accessed February 25, 2020. https://ir.uiowa.edu/etd/5518.

MLA Handbook (7^th Edition):

Janowski, Ann M. “The protective roles of NLRs during infection and tumor progression.” 2016. Web. 25 Feb 2020.

Vancouver:

Janowski AM. The protective roles of NLRs during infection and tumor progression. [Internet] [Doctoral dissertation]. University of Iowa; 2016. [cited 2020 Feb 25]. Available from: https://ir.uiowa.edu/etd/5518.

Council of Science Editors:

Janowski AM. The protective roles of NLRs during infection and tumor progression. [Doctoral Dissertation]. University of Iowa; 2016. Available from: https://ir.uiowa.edu/etd/5518

25. Liu, Runxia. Genetic Interference and Receptor Biology of Neglected Influenza Viruses.

Degree: PhD, Biology and Microbiology, 2017, South Dakota State University

URL: https://openprairie.sdstate.edu/etd/2157

► Influenza B virus (IBV) is an important pathogen that infects humans and causes seasonal influenza epidemics. By using next-generation sequencing (NGS) approach, we analyzed… (more)

▼ Influenza B virus (IBV) is an important pathogen that infects humans and causes seasonal influenza epidemics. By using next-generation sequencing (NGS) approach, we analyzed total mRNAs extracted from A549 cells infected with B/Brisbane/60/2008, and identified four defective genomes in IBV with two from the polymerase basic subunit 1 (PB1) segment and the other two from the matrix (M) segment. Each of them can potently inhibit the replication of IBV. One derived from PB1 segment was able to interfere modestly with influenza A virus (IAV) replication. The productions of the four defective RNAs are not dependent on the cell types. The important initial insights into IBV defective genomes can be further explored toward better understanding of the replication, pathogenesis, and evolution of IBV. The second study demonstrated that influenza D virus (IDV) is more efficient in recognizing both human Neu5,9Ac2 and non-human Neu5Gc9Ac receptors than influenza C virus (ICV). ICV prefers human Neu5,9Ac2 over non-human Neu5Gc9Ac. The results reveal that IDV and ICV diverge in communicating with both O-acetyl group at the C9 position and acetyl/glycolyl groups at the C5 position in terminal 9-carbon SAs. Our findings provide evidence that IDV has acquired the unique ability to infect and transmit among agricultural animals that are enriched in Neu5Gc9Ac, in addition to pose a zoonotic risk to humans only expressing Neu5,9Ac2. Characterization of a contemporary human ICV is needed. C/Victoria/2/2012 (C/Vic) isolated in 2012 was used in this study. Phylogenetic studies demonstrated that C/Vic is a reassortant virus composed of segments derived from multiple ICV lineages or strains, which evolved independently. We identified two mutations in the 170-loop of the HEF protein around the receptor binding pocket as a possible antigenic determinant responsible for the discrepant hemagglutinin inhibition results. C/Vic replicates more efficiently at the cool temperature, which should be further investigated toward elucidating the molecular determinants of temperature-dependent growth. The study on this contemporary ICV shall aid in the further investigation of biology, evolution, and pathogenesis of ICV. Advisors/Committee Members: Feng Li.

Subjects/Keywords: Immunology and Infectious Disease; Microbiology; Virology

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APA (6^th Edition):

Liu, R. (2017). Genetic Interference and Receptor Biology of Neglected Influenza Viruses. (Doctoral Dissertation). South Dakota State University. Retrieved from https://openprairie.sdstate.edu/etd/2157

Chicago Manual of Style (16^th Edition):

Liu, Runxia. “Genetic Interference and Receptor Biology of Neglected Influenza Viruses.” 2017. Doctoral Dissertation, South Dakota State University. Accessed February 25, 2020. https://openprairie.sdstate.edu/etd/2157.

MLA Handbook (7^th Edition):

Liu, Runxia. “Genetic Interference and Receptor Biology of Neglected Influenza Viruses.” 2017. Web. 25 Feb 2020.

Vancouver:

Liu R. Genetic Interference and Receptor Biology of Neglected Influenza Viruses. [Internet] [Doctoral dissertation]. South Dakota State University; 2017. [cited 2020 Feb 25]. Available from: https://openprairie.sdstate.edu/etd/2157.

Council of Science Editors:

Liu R. Genetic Interference and Receptor Biology of Neglected Influenza Viruses. [Doctoral Dissertation]. South Dakota State University; 2017. Available from: https://openprairie.sdstate.edu/etd/2157

Loyola University Chicago

26. Zook, Erin Christine. Promoting Thymopoiesis with Age: Potential Role of the Transcription Factor Foxn1.

Degree: PhD, Cell Biology, Neurobiology and Anatomy, 2012, Loyola University Chicago

URL: https://ecommons.luc.edu/luc_diss/317

► It is known that the elderly are more susceptible to illnesses and infections and respond poorly to immunization. A contributing factor to a decrease… (more)

▼ It is known that the elderly are more susceptible to illnesses and infections and respond poorly to immunization. A contributing factor to a decrease in the immune response in the elderly is the decline in the production of naïve T cell by the thymus. In the thymus, the notch receptor expressed on early T cell progenitors (ETP) binds to its ligand expressed on thymic epithelial cells (TEC), signaling ETP to develop through a series of developmental stages before maturing into naive T cells. Because ETP are non-self renewing, the thymus relies on the bone marrow (BM) for a continuous supply of T cell progenitors to generate and maintain the peripheral T cell pool. With age, the numbers of TEC, ETP, as well as the number of T cell progenitors in the BM are reduced, contributing to the decline in the production of naïve T cells. Previously, our lab has shown that with age, the decline in the number of thymocytes correlates with the decline in the expression of Foxn1 in thymic stroma. Foxn1 is a transcription factor critical for functional maturation of TEC and thymic organogenesis. Mutations in Foxn1 result in the nude phenotype characterized by hairless and athymic conditions. Interestingly, nude mice also have defects in the BM, suggesting a role for Foxn1 in hematopoiesis. A Foxn1Tg mouse model was developed in which Foxn1 is over expressed in thymus and in the BM. I showed that aged Foxn1Tg mice have a higher number of TEC, and ETP; consequently, leading to attenuation of the age-associated decline in thymopoiesis. In addition, the decline in the number of bone marrow-derived T cell progenitors is prevented in Foxn1Tg. Using adaptive transfer experiments, I demonstrated that the aged Foxn1Tg BM microenvironment promotes the development of T cell progenitors. Lastly, I have identified a novel population of cells in the BM that express Foxn1. Taken together this data suggests that the presence of Foxn1 expressing cells in the thymus and BM contribute to niches that play an important role in the maintenance of T cell progenitors with age.

Subjects/Keywords: Aging; Foxn1; Thymus; Immunology and Infectious Disease

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APA (6^th Edition):

Zook, E. C. (2012). Promoting Thymopoiesis with Age: Potential Role of the Transcription Factor Foxn1. (Doctoral Dissertation). Loyola University Chicago. Retrieved from https://ecommons.luc.edu/luc_diss/317

Chicago Manual of Style (16^th Edition):

Zook, Erin Christine. “Promoting Thymopoiesis with Age: Potential Role of the Transcription Factor Foxn1.” 2012. Doctoral Dissertation, Loyola University Chicago. Accessed February 25, 2020. https://ecommons.luc.edu/luc_diss/317.

MLA Handbook (7^th Edition):

Zook, Erin Christine. “Promoting Thymopoiesis with Age: Potential Role of the Transcription Factor Foxn1.” 2012. Web. 25 Feb 2020.

Vancouver:

Zook EC. Promoting Thymopoiesis with Age: Potential Role of the Transcription Factor Foxn1. [Internet] [Doctoral dissertation]. Loyola University Chicago; 2012. [cited 2020 Feb 25]. Available from: https://ecommons.luc.edu/luc_diss/317.

Council of Science Editors:

Zook EC. Promoting Thymopoiesis with Age: Potential Role of the Transcription Factor Foxn1. [Doctoral Dissertation]. Loyola University Chicago; 2012. Available from: https://ecommons.luc.edu/luc_diss/317

27. Tranchemontagne, Zachary Ronald. Community-Acquired Methicillin-Resistant Staphylococcus Aureus (CA-MRSA) USA300 Perturbs Acquisition Of Lysosomal Hydrolases And Requires Phagosomal Acidification For Survival In A Human Macrophage Cell Line.

Degree: MSin Biological Sciences, Biological Science, 2015, University of New England

URL: https://dune.une.edu/theses/99

► Community-acquired Methicillin-resistant Staphylococcus aureus (CA-MRSA) strain USA300 is a major cause of invasive drug-resistant skin and soft tissue infections in humans. Although S. aureus… (more)

Subjects/Keywords: Biology; Immunology and Infectious Disease; Microbiology

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APA (6^th Edition):

Tranchemontagne, Z. R. (2015). Community-Acquired Methicillin-Resistant Staphylococcus Aureus (CA-MRSA) USA300 Perturbs Acquisition Of Lysosomal Hydrolases And Requires Phagosomal Acidification For Survival In A Human Macrophage Cell Line. (Thesis). University of New England. Retrieved from https://dune.une.edu/theses/99

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):

Tranchemontagne, Zachary Ronald. “Community-Acquired Methicillin-Resistant Staphylococcus Aureus (CA-MRSA) USA300 Perturbs Acquisition Of Lysosomal Hydrolases And Requires Phagosomal Acidification For Survival In A Human Macrophage Cell Line.” 2015. Thesis, University of New England. Accessed February 25, 2020. https://dune.une.edu/theses/99.

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

MLA Handbook (7^th Edition):

Tranchemontagne, Zachary Ronald. “Community-Acquired Methicillin-Resistant Staphylococcus Aureus (CA-MRSA) USA300 Perturbs Acquisition Of Lysosomal Hydrolases And Requires Phagosomal Acidification For Survival In A Human Macrophage Cell Line.” 2015. Web. 25 Feb 2020.

Vancouver:

Tranchemontagne ZR. Community-Acquired Methicillin-Resistant Staphylococcus Aureus (CA-MRSA) USA300 Perturbs Acquisition Of Lysosomal Hydrolases And Requires Phagosomal Acidification For Survival In A Human Macrophage Cell Line. [Internet] [Thesis]. University of New England; 2015. [cited 2020 Feb 25]. Available from: https://dune.une.edu/theses/99.

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

Council of Science Editors:

Tranchemontagne ZR. Community-Acquired Methicillin-Resistant Staphylococcus Aureus (CA-MRSA) USA300 Perturbs Acquisition Of Lysosomal Hydrolases And Requires Phagosomal Acidification For Survival In A Human Macrophage Cell Line. [Thesis]. University of New England; 2015. Available from: https://dune.une.edu/theses/99

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

University of Iowa

28. Thalhofer, Colin Joseph. Leishmania infantum chagasi induces a dynamic cellular inflammatory response.

Degree: PhD, Immunology, 2011, University of Iowa

URL: https://ir.uiowa.edu/etd/1091

► Leishmania infantum chagasi (Lic) is a pathogenic protozoan parasite and one of the etiological agents of human visceral leishmaniasis (VL). VL is a potentially… (more)

▼ Leishmania infantum chagasi (Lic) is a pathogenic protozoan parasite and one of the etiological agents of human visceral leishmaniasis (VL). VL is a potentially deadly disease characterized by variable fevers, cachexia, hepatosplenomegaly, and global immune suppression. Many questions regarding the pathogenesis of VL and the mechanisms of host defense during Lic infection remain to be elucidated. The primary focus of this thesis is the relationship between Lic and the mammalian immune system. We studied parasite-host interactions during Lic infection at the molecular, cellular, and organismal level. We generated transgenic parasites that expressed firefly luciferase and/or fluorescent proteins to expand our capacity to detect, observe, and quantify the parasites in a variety of experimental settings with modern analytical methodologies. Using luciferase-expressing Leishmania, we developed an experimental infection model in which parasites were detected and the relative parasite burden in specific anatomical locations could be quantified in a live animal host using bioluminescence imaging. This method allowed the parasite burden to be assessed in the same host throughout the course of infection. Utilizing this model we have made some intriguing observations relating to the kinetics and distribution of the parasite burden over time. The parasite burden was observed primarily in the liver and bone marrow over the first few weeks and then shifts to the spleen and bone marrow. To gain a better understanding of the initial parasite-host immune interactions in vivo, we studied the early inflammatory response after intradermal (i.d.) inoculation. We observed a rapid and abundant influx of neutrophils into the inoculated ears. The neutrophil influx was transient, dose dependent and specific for the local inoculation site. While there was not a significant neutrophil influx into the draining lymph nodes (dLN), there was an increase in the total cellularity and a striking increase in the relative proportion of B cells to T cells over the first week after intradermal parasite challenge. By inoculating transgenic mCherry-Lic we found that neutrophils were the primary parasite-laden host cell in the dermal tissue during the first day, but macrophages harbored most of the parasites by 2 days. Neutrophil depletion using low-dose antibody treatment resulted in a reduced rate of parasite uptake initially at the site of inoculation, but no significant change in the dLN dynamics. We further examined the parasite-host relationship by studying molecular signaling and cellular interactions between Leishmania and human neutrophils. We investigated the nature of the chemotactic activity of Leishmania-conditioned growth medium for human neutrophils by testing physical properties of the activity and ruled out some of the major Leishmania surface molecules as potential candidates. We aim to identify the agent(s) responsible for the activity in on-going studies. To this end, we are collaborating with a… Advisors/Committee Members: Wilson, Mary E. (supervisor).

Subjects/Keywords: Leishmania; Neutrophil; Immunology of Infectious Disease

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

APA (6^th Edition):

Thalhofer, C. J. (2011). Leishmania infantum chagasi induces a dynamic cellular inflammatory response. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/1091

Chicago Manual of Style (16^th Edition):

Thalhofer, Colin Joseph. “Leishmania infantum chagasi induces a dynamic cellular inflammatory response.” 2011. Doctoral Dissertation, University of Iowa. Accessed February 25, 2020. https://ir.uiowa.edu/etd/1091.

MLA Handbook (7^th Edition):

Thalhofer, Colin Joseph. “Leishmania infantum chagasi induces a dynamic cellular inflammatory response.” 2011. Web. 25 Feb 2020.

Vancouver:

Thalhofer CJ. Leishmania infantum chagasi induces a dynamic cellular inflammatory response. [Internet] [Doctoral dissertation]. University of Iowa; 2011. [cited 2020 Feb 25]. Available from: https://ir.uiowa.edu/etd/1091.

Council of Science Editors:

Thalhofer CJ. Leishmania infantum chagasi induces a dynamic cellular inflammatory response. [Doctoral Dissertation]. University of Iowa; 2011. Available from: https://ir.uiowa.edu/etd/1091

University of Louisville

29. Guha Niyogi, Rajarshi. Cannabinoids suppress the innate immune response to periodontal pathogen Porphyromonas gingivalis in gingival epithelial cells.

Degree: MS, 2016, University of Louisville

URL: 10.18297/etd/2503 ; https://ir.library.louisville.edu/etd/2503

► Marijuana is widely used in the United States for recreational and medicinal purposes. Despite the proposed beneficial effects of cannabis on certain medical conditions,… (more)

▼ Marijuana is widely used in the United States for recreational and medicinal purposes. Despite the proposed beneficial effects of cannabis on certain medical conditions, there is also a concern there is also a concern over negative health consequences of marijuana smoking. Recently, cannabis use has been established as a dose related risk factor for chronic periodontitis. Although the induction / exacerbation of chronic periodontitis in marijuana users has been established epidemiologically, the mechanisms underlying such predisposition are still unknown. It has long been suggested that marijuana has anti-inflammatory properties, while human epithelial cells are known to express cannabinoid receptor type 2 (CB2). Therefore, we hypothesized that marijuana-derived cannabinoids may suppress the innate immune response, altering the ability of gingival epithelial cells to respond appropriately to bacterial stimuli (the classic TLR4 ligand, E. coli LPS; and the major periodontal vii pathogen, Porphyromonas gingivalis). More specifically, we hypothesized that predominant phytocannabinoid subtypes (cannabidiol [CBD], cannabinol [CBN], or tetrahydrocannabinol [THC]) at physiologically relevant doses (0 - 10µg/ml) would suppress proinflammatory cytokine production in LPS- (0-1µg/ml) or P. gingivalis (MOI, 10:1) exposed telomerase immortalized human gingival keratinocytes (TIGK cells) in a CB2-related manner. We also hypothesized that marijuana-derived cannabinoids may influence the viability of both epithelial (TIGK cells, as assessed by Trypan blue exclusion) and representative oral bacteria (P. gingivalis, Treponema denticola and Filifactor alocis, growth curves monitored by optical density). Higher doses (>5 µg/ml) of marijuana derived cannabinoids (CBD, CBN or THC) inhibited the growth of P. gingivalis (p < 0.001) and F. alocis (p < 0.001), relative to unexposed bacteria, whereas T. denticola growth was resistant to all cannabinoid doses tested (1- 10 µg/ml, p > 0.05).. TIGK cells were non-viable when exposed to high cannabinoid concentrations (> 10 µg/ml).Sub-lethal (1 -5 µg/ml) doses of each cannabinoid subtype suppressed the production of IL-8 and IL-6 but enhanced IL-10 release in P. gingivalis or LPS stimulated TIGKs (all p < 0.001). Treatment with the CB2 inhibitor, JTE907, did not rescue cannabinoid-induced immune suppression, suggesting that alternative cannabinoid receptors, such as CB1, GPR55 or A2A receptors, may be associated with the anti YLLL inflammatory function of marijuana-derived cannabinoids. If the phenomena of (i) cannabinoid induced epithelial toxicity; (ii) growth restriction of a sub-population of bacterial species in the oral biofilm; and (iii) innate suppression in gingival epithelial cells, established herein, occur in vivo, they are likely to help explain increased susceptibility to periodontal diseases in cannabis users. To expand, the epithelial barrier may be compromised in marijuana smokers, facilitating bacterial entry and more efficient diffusion of microbial toxins into the gingival… Advisors/Committee Members: Scott, David, Lamont, Richard, Lamont, Richard, Wang, Huizi.

Subjects/Keywords: cannabinoids; inaate immunity; P. gingivalis; chronic periodontitis; Immunology and Infectious Disease; Immunology of Infectious Disease

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

APA (6^th Edition):

Guha Niyogi, R. (2016). Cannabinoids suppress the innate immune response to periodontal pathogen Porphyromonas gingivalis in gingival epithelial cells. (Masters Thesis). University of Louisville. Retrieved from 10.18297/etd/2503 ; https://ir.library.louisville.edu/etd/2503

Chicago Manual of Style (16^th Edition):

Guha Niyogi, Rajarshi. “Cannabinoids suppress the innate immune response to periodontal pathogen Porphyromonas gingivalis in gingival epithelial cells.” 2016. Masters Thesis, University of Louisville. Accessed February 25, 2020. 10.18297/etd/2503 ; https://ir.library.louisville.edu/etd/2503.

MLA Handbook (7^th Edition):

Guha Niyogi, Rajarshi. “Cannabinoids suppress the innate immune response to periodontal pathogen Porphyromonas gingivalis in gingival epithelial cells.” 2016. Web. 25 Feb 2020.

Vancouver:

Guha Niyogi R. Cannabinoids suppress the innate immune response to periodontal pathogen Porphyromonas gingivalis in gingival epithelial cells. [Internet] [Masters thesis]. University of Louisville; 2016. [cited 2020 Feb 25]. Available from: 10.18297/etd/2503 ; https://ir.library.louisville.edu/etd/2503.

Council of Science Editors:

Guha Niyogi R. Cannabinoids suppress the innate immune response to periodontal pathogen Porphyromonas gingivalis in gingival epithelial cells. [Masters Thesis]. University of Louisville; 2016. Available from: 10.18297/etd/2503 ; https://ir.library.louisville.edu/etd/2503

University of Pennsylvania

30. Whitmarsh, Ryan J. Innate Signals in the Macrophage Determine the Severity of Toxoplasma Gondii infection.

Degree: 2011, University of Pennsylvania

URL: https://repository.upenn.edu/edissertations/433

► Toxoplasma gondii is an obligate intracellular pathogen that is a cause of significant morbidity and mortality in humans and animals. The immune response necessary to… (more)

▼ Toxoplasma gondii is an obligate intracellular pathogen that is a cause of significant morbidity and mortality in humans and animals. The immune response necessary to control this infection requires successful coordination of strong innate and adaptive responses. Recognition of the pathogen by innate accessory cells such as macrophages, neutrophils, and dendritic cells induces the release of IL-12 that activates NK and T cells to produce protective IFN-g, the major mediator of immunity to T. gondii. T. gondii has many mechanisms to limit the activation of innate cells and to reduce the production of IL-12. One of the ways T. gondii achieves this is by inducing the phosphorylation of the transcription factor Signal Transducer of Activation 3 (STAT3) that leads to repressed pro-inflammatory responses such as diminished IL-12 production. How STAT3 antagonizes inflammatory responses is poorly understood but the Suppressors of Cytokine Signaling (SOCS) proteins are downstream candidate molecules that antagonize cytokine signaling. Recent studies have identified SOCS proteins as being important during infection with a number of pathogens and have provided insights into how intracellular pathogens affect STAT signaling to promote their replication and survival. In particular, SOCS1 is thought to inhibit IFN-g signals whereas SOCS3 antagonizes IL-6 signals. Studies have shown that both of these proteins are upregulated in other models but little is known about how they contribute to the outcome of infection. This thesis provides evidence that the IL-6 signaling in macrophages reduces the cell’s ability to produce IL-12 that is enhanced in the absence of SOCS3. Furthermore, infection of SOCS3 conditional knockouts leads to acute susceptibility with high parasite burdens associated with impaired IL-12 production. Blocking anti-bodies to IL-6 as well as addition of exogenous IL-12 rescues the lethality in these mice suggesting that IL-6 is a natural antagonist of IL-12 production during infection with T. gondii. This thesis will discuss the roles that IL-6, STAT3, and SOCS3 play during infection with T. gondii and how these molecules affect cytokine regulation, cellular recruitment, and microbicidal activity and also how these studies enhance our understanding of inflammation and resistance to infection.

Subjects/Keywords: Toxoplasma; macrophage; SOCS3; STAT3; Immunology of Infectious Disease; Immunopathology; Other Immunology and Infectious Disease; Parasitology

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

APA (6^th Edition):

Whitmarsh, R. J. (2011). Innate Signals in the Macrophage Determine the Severity of Toxoplasma Gondii infection. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/433

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):

Whitmarsh, Ryan J. “Innate Signals in the Macrophage Determine the Severity of Toxoplasma Gondii infection.” 2011. Thesis, University of Pennsylvania. Accessed February 25, 2020. https://repository.upenn.edu/edissertations/433.

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

MLA Handbook (7^th Edition):

Whitmarsh, Ryan J. “Innate Signals in the Macrophage Determine the Severity of Toxoplasma Gondii infection.” 2011. Web. 25 Feb 2020.

Vancouver:

Whitmarsh RJ. Innate Signals in the Macrophage Determine the Severity of Toxoplasma Gondii infection. [Internet] [Thesis]. University of Pennsylvania; 2011. [cited 2020 Feb 25]. Available from: https://repository.upenn.edu/edissertations/433.

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

Council of Science Editors:

Whitmarsh RJ. Innate Signals in the Macrophage Determine the Severity of Toxoplasma Gondii infection. [Thesis]. University of Pennsylvania; 2011. Available from: https://repository.upenn.edu/edissertations/433

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

Open Access Theses and Dissertations