Gastrointestinal (Gl) diseases affect over 70 million people in the United States annually. In 1992, the collective medical costs of Gl diseases was reported to be in excess of $100 billion in the US alone. Inflammatory Bowel Disease (IBD) is a chronic inflammatory disease of the Gl tract and the etiology is unknown. Resident intestinal bacteria have been implicated in the pathogenesis of IBD as evidenced by the resistance of germfree mice to many forms of colitis in comparison to colitis observed in mice bearing a conventional microflora. Preliminary data shows that colonization of gnotobiotic mice with Helicobacter bilis induces antigen-specific responses to members of the resident flora. We propose that a disruption of the microbial ecology of the Gl tract induces aberrant immune responses directed at luminal antigens, resulting in an increased susceptibility to colitis. To test this hypothesis, we will inoculate gnotobiotic mice with H.bilis and evaluate their susceptibility to a colitic insult (low dose dextran sulfate sodium, DSS). Comparisons in disease severity and immune responses will be assessed between groups. Results from these studies will add to our understanding of the host-flora interactions that contribute to the susceptibility to colitis. ? ?
