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Please use this identifier to cite or link to this item: http://hdl.handle.net/11375/13491
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dc.contributor.advisorVerdu, Elena F.en_US
dc.contributor.advisorStephen Collins and Manel Jordanaen_US
dc.contributor.authorNatividad, Jane Mea M.en_US
dc.date.accessioned2014-06-18T17:04:12Z-
dc.date.available2014-06-18T17:04:12Z-
dc.date.created2013-09-25en_US
dc.date.issued2013-10en_US
dc.identifier.otheropendissertations/8322en_US
dc.identifier.other9460en_US
dc.identifier.other4631390en_US
dc.identifier.urihttp://hdl.handle.net/11375/13491-
dc.description.abstract<p>Intestinal microbiota are key determinants of gut homeostasis and affect various gut physiological and immune processes. Co-evolution has enabled the host and intestinal microbes to exist in a mutualistic relationship. However, interactions between the host and its intestinal microbiota exist in a delicate balance between mutualism and pathogenicity. Maintenance or disruption of this balance depends on a complex interplay between the microbiota and the host, as well as other gut luminal factors, including diet, that are poorly understood. The main goal of this thesis has been to study the host-gut luminal interactions that regulate gut physiology and immunity. In particular, <strong>Chapter 2</strong> centers on investigating the effect of perturbing the intestinal barrier using a non-steroidal inflammatory drug on host-microbial and dietary interactions in a mouse model of gluten sensitivity. I demonstrated that indomethacin-induced increase in intestinal permeability is associated with altered intestinal microbiota composition, systemic antibody development against intestinal bacteria and a shift in immune responses to the dietary antigen, gluten. <strong>Chapter 3</strong> focuses on investigating whether modulation of the intestinal microbiota can affect the host’s susceptibility to intestinal injury. I used mice with defective intracellular bacterial receptor signaling because discrimination between commensals and pathogens is, in part, achieved by a family of receptors that recognize conserved bacterial components. I demonstrated that the microbiota with which these mice are colonized influences the expression of RegIII-γ, a type of antimicrobial peptide, and susceptibility to intestinal injury. To gain further insight on the effect of microbiota on antimicrobial peptides, in <strong>Chapter 4</strong> we conducted a combination of gnotobiotic and <em>in-vitro</em> experiments where we identified that specific components of the microbiota differentially regulate RegIII expression. Further examination showed that <em>MyD88 a</em>nd <em>Ticam1 </em>genes, which are signaling adaptor proteins of pattern recognition receptors, are essential regulators of microbial–induced RegIII expression by intestinal epithelial cells. Collectively, the work presented in this thesis provides novel insight on the bi-directional interaction between the host and the gut luminal content as well as of potential beneficial effects of microbiota-modulating strategies in maintaining homeostasis and preventing disease.</p>en_US
dc.subjectIntestinal microbiotaen_US
dc.subjectCeliac diseaseen_US
dc.subjectInflammatory Bowel Diseaseen_US
dc.subjectIntestinal immunity and homeostasisen_US
dc.subjectIntestinal inflammationen_US
dc.subjectProbioticsen_US
dc.subjectDigestive, Oral, and Skin Physiologyen_US
dc.subjectDigestive, Oral, and Skin Physiologyen_US
dc.titleThe Role of Intestinal Microbiota on the Regulation of Gut Function and Immunityen_US
dc.typethesisen_US
dc.contributor.departmentHealth Sciencesen_US
dc.description.degreeDoctor of Philosophy (Medical Science)en_US
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