Theses and Dissertations at Montana State University (MSU)
Permanent URI for this collectionhttps://scholarworks.montana.edu/handle/1/733
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Item Heligmosomoides polygyrus infection : the role of cytokines in regulation of mast cell development(Montana State University - Bozeman, College of Agriculture, 1995) Hall-Stoodley, LuanneItem The Staphylococcus aureus two-component system, SAER/S, modulates host mediators of inflammation to enhance pathogenesis(Montana State University - Bozeman, College of Agriculture, 2013) Watkins, Robert Lee; Chairperson, Graduate Committee: Jovanka Voyich-Kane; Kyler B Pallister and Jovanka M Voyich were co-authors of the article, 'The SAER/S gene regulatory system induces a proinflammatory cytokine response during Staphylococcus aureus infection' in the journal 'PLoS one' which is contained within this thesis.; Oliwia W Zurek, Kyler B Pallister and Jovanka M Voyich were co-authors of the article, 'The SAER/S two-component system promotes interferon-gamma in neutrophils during invasive Staphylococcus aureus infection' submitted to the journal 'Microbes and infection' which is contained within this thesis.; Oliwia W Zurek, Kyler B Pallister and Jovanka M Voyich were co-authors of the article, 'The SAER/S virulence system promotes interferon-gamma to enhance Staphylococcus aureus skin disease in an interleukin-17-dependent manner' submitted to the journal 'Journal of infectious diseases' which is contained within this thesis.Methicillin-resistant Staphylococcus aureus (MRSA) is an opportunistic pathogen that causes diseases ranging from superficial skin infections to life-threatening invasive disease. The emergence of community-associated MRSA has caused concern, as these infections appear in healthy individuals. Increasing prevalence of antimicrobial resistance warrants the development of alternative methods of combating infections. Modulating the host immune response during infection has shown promise in research settings, but has fallen short of application in the clinic. Characterizing how Staphylococcus aureus (S. aureus) influences host mediators of inflammation is an essential step for understanding S. aureus pathogenesis and could lead to the development of novel therapies, including immuno-modulation. Previous studies demonstrated the SaeR/S two-component system of S. auerus strongly regulates exoprotein production and is essential for full virulence of this pathogen. However, the mechanisms behind the role(s) of SaeR/S in mediating pathogenesis are incompletely defined. To that end, this investigation examined the role SaeR/S in impacting host inflammatory responses during both invasive and superficial S. aureus infections. Using mutant S. aureus strains with deleted saeR/S (DeltasaeR/S), these studies show that SaeR/S is critical for promoting pathogen survival, dissemination and host mortality during peritonitis. Pro-inflammatory cytokines, such as interferon-gamma (IFNgamma), tumor necrosis factor-alpha and interleukin (IL)-6 were significantly reduced in mice infected with DeltasaeR/S. IFNgamma transcriptional activation and protein expression were significantly induced by saeR/S during skin and invasive infections. Interestingly, neutrophils were identified as the predominant source of saeR/S-induced IFNgamma expression during early S. aureus peritonitis. Robust saeR/S-influenced IFNgamma production prompted further studies investigating the role of this cytokine during S. aureus infections. IFNgamma-deficient (GKO) mice were protected during invasive infection with wild-type S. aureus as reduced bacterial burdens and reduced host cellular cytotoxicity were observed. GKO mice were protected against wild-type S. aureus skin challenge in an IL-17-dependent manner. Interestingly, both normal and GKO mice exhibited similar pathologies when infected with DeltasaeR/S during invasive and superficial infections, suggesting that IFNgamma and IL-17 impact saeR/S-mediated pathogenesis and that in the absence of saeR/S, these cytokines are inconsequential in mediating immunity. Collectively, these studies suggest that saeR/S promotes a deleterious IFNgamma response that enhances S. aureus pathogenesis.Item Do carbohydrates increase the magnitude of the inflammatory response(Montana State University - Bozeman, College of Education, Health & Human Development, 2008) Depner, Chris M.; Chairperson, Graduate Committee: Mary P. Miles.Inflammation is the body's response to tissue damage and infection and is correlated with several chronic diseases like type II diabetes. Cytokines are cell signaling proteins with multiple functions including control of inflammation. Cytokines are influenced by several factors such as carbohydrate intake and exercise. Thus, carbohydrate intake and exercise can influence inflammation. Purpose: To determine the influence of high carbohydrate intake on the inflammatory response to exercise that induces muscle damage and inflammation. Methods: The study was a cross-over design. Each subject completed a high carbohydrate condition and a high fat and protein condition. Each condition consisted of 6 sets of 10 maximal high-force eccentric contractions of the elbow flexors and extensors. The exercise was followed by a controlled diet for the first 8 hours post-exercise based on the condition. The cytokines interleukin-6 (IL-6) and interleukin-1B (IL-B) were measured as indicators of local inflammation. C-reactive protein (CRP) was measured as an indicator of systemic inflammation. Creatine-kinase (CK), muscle soreness, upper arm circumference, and strength loss were measured as indicators of muscle damage. Blood glucose and insulin were measured to identify differences between diets in the conditions. Results: Insulin was significantly increased in the high carbohydrate condition compared to the high fat and protein condition at 1.5, 4, and 8 hours post-exercise. Perceived soreness was elevated at all time points post-exercise in both conditions and was significantly elevated in the high carbohydrate condition compared to the high fat and protein condition. There was a main effect trend for IL-6 to be greater in the high carbohydrate condition compared to the high fat and protein condition. Il-1B was significantly increased 24 hours post-exercise in the high carbohydrate condition compared to the high fat and protein condition. Conclusion: Elevated carbohydrate intake post-exercise augmented the local inflammatory response to the exercise observed by elevated IL-1B and IL-6. The augmented inflammatory response contributed to greater perceived muscle soreness post-exercise. Further research is required to investigate this mechanism further to provide better prevention and treatment methods for chronic diseases related to inflammation.