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Current research indicates that inflammatory bowel diseases (IBD’s), including Crohn’s disease and ulcerative colitis, are due to uncontrolled innate and adaptive immune responses to commensal (non-pathogenic) intestinal bacteria in genetically susceptible hosts. However, the roles of intestinal bacteria in the perpetuation and progression of IBD’s are unclear and the effects of intestinal inflammation on commensal bacterial physiology and virulence are unknown. We hypothesize that commensal bacteria dynamically respond to intestinal inflammation in a manner that perpetuates or worsens disease. Exploring this hypothesis will enhance our understanding of the pathogenesis of IBD’s and host-microbial interactions, and potentially identify new therapeutic targets for these currently incurable diseases.,Current research indicates that inflammatory bowel diseases (IBD’s), including Crohn’s disease and ulcerative colitis, are due to uncontrolled innate and adaptive immune responses to commensal (non-pathogenic) intestinal bacteria in genetically susceptible hosts. However, the roles of intestinal bacteria in the perpetuation and progression of IBD’s are unclear and the effects of intestinal inflammation on commensal bacterial physiology and virulence are unknown. We hypothesize that commensal bacteria dynamically respond to intestinal inflammation in a manner that perpetuates or worsens disease. Exploring this hypothesis will enhance our understanding of the pathogenesis of IBD’s and host-microbial interactions, and potentially identify new therapeutic targets for these currently incurable diseases.
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UNC AFFILIATIONS:
Center for GI Biology and Disease (CGIBD), Department of Medicine (DOM), Microbiology & Immunology |
CLINICAL/RESEARCH INTERESTS:
Bacteriology, Immunology, Pathogenesis & Infection, Translational Medicine |