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dc.contributor.advisorFranklin, Craig L.eng
dc.contributor.authorHillhouse, Andrew Edwardeng
dc.date.issued2010eng
dc.date.submitted2010 Falleng
dc.descriptionThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.eng
dc.descriptionTitle from PDF of title page (University of Missouri--Columbia, viewed on March 11, 2011).eng
dc.descriptionIncludes bibliographical referenceseng
dc.descriptionVita.eng
dc.descriptionThesis advisor: Craig L. Franklin.eng
dc.description"December 2010"eng
dc.descriptionPh. D. University of Missouri-Columbia 2010.eng
dc.descriptionDissertations, Academic -- University of Missouri--Columbia -- Molecular microbiology & immunology.eng
dc.description.abstractInflammatory Bowel Diseases (IBDs) affect millions of people worldwide and are characterized by a chronic intestinal inflammation resulting from a dysregulated immune response to environmental stimuli in genetically susceptible individuals. Utilizing a mouse model of IBD, the studies presented herein investigated 1) the role for estrogen and estrogen receptors in disease development 2) genetic factors contributing to differential disease susceptibility 3) differences in bacterial flora between susceptible and resistant mice. Infection of the A/J mouse strain with the bacterium Helicobacter hepaticus results in acute over-expression of proinflammatory cytokines followed 2-3 months later by chronic cecal inflammation that is more severe in females than in males. Studies in these mice investigating the role for estrogen and estrogen receptors have revealed that selective signaling through estrogen receptor [beta] is immunomodulatory and decreases intestinal inflammation. Helicobacter hepaticus infected A/J mice develop intestinal inflammation, but infected C57BL/6 mice do not. Our investigations into the genetic factors responsible for Helicobacter hepaticus-induced intestinal inflammation have identified two major quantitative trait loci (QTL) on chromosome 3 and 17 associated with disease susceptibility. We also show that the microbial flora between these two mouse strains differs and can impact disease susceptibility. Together the work presented herein a further understanding into the role of hormones in controlling inflammation and insight into the genetic and bacterial factors associated with disease susceptibility.eng
dc.format.extentxi, 122 pageseng
dc.identifier.oclc707080673eng
dc.identifier.urihttps://hdl.handle.net/10355/10292
dc.identifier.urihttps://doi.org/10.32469/10355/10292eng
dc.languageEnglisheng
dc.publisher[University of Missouri--Columbia]eng
dc.relation.ispartofcollectionUniversity of Missouri--Columbia. Graduate School. Theses and Dissertationseng
dc.relation.ispartofcommunityUniversity of Missouri-Columbia. Graduate School. Theses and Dissertations. Dissertations. 2010 Dissertationseng
dc.subject.meshInflammatory Bowel Diseases -- immunologyeng
dc.subject.meshInflammatory Bowel Diseases -- geneticseng
dc.subject.meshEstrogens -- Metabolismeng
dc.subject.meshEstrogen Receptor beta -- Metabolismeng
dc.subject.meshEstrogen receptor beta -- Immunologyeng
dc.subject.meshIntestinal mucosa -- Microbiologyeng
dc.subject.meshHelicobacter hepaticus -- Immunologyeng
dc.subject.meshHelicobacter hepaticus -- Geneticseng
dc.subject.meshHelicobacter infections -- Immunologyeng
dc.subject.meshHelicobacter infections -- Geneticseng
dc.subject.meshMiceeng
dc.titleHormonal and genetic regulation of Helicobacter hepaticus-induced intestinal inflammationeng
dc.typeThesiseng
thesis.degree.disciplineMolecular microbiology and immunology (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelDoctoraleng
thesis.degree.namePh. D.eng


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