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Irritable Bowel Syndrome (IBS) is one of the most common chronic medical conditions, affecting 10%-15% of the population in the United States and worldwide. Work on two distinct fronts has suggested that the pathophysiology of IBS may have microbial origins. First, a series of studies and meta-analyses over the last decade suggests that IBS can develop after a single episode of acute bacterial gastroenteritis (referred to as post-infectious IBS (PI-IBS). While these subjects exhibit characteristic gut immunologic changes (in the mucosa and myenteric ganglia), the mechanisms underlying the transition to an IBS phenotype remain unknown. Second, subjects with IBS have been shown to have specific changes in luminal bacterial contents, the most common of which is small intestinal bacterial overgrowth (SIBO), a condition whereby coliform bacterial counts in the small bowel become excessive. The presence of SIBO in IBS subjects has recently been confirmed by both small bowel culture and by quantitative PCR (qPCR) of duodenal contents.
The focus of our research is on the association between acute gastroenteritis and disruption of gut flora, impairment of GI tract motility, and small intestinal bacterial overgrowth in the pathophysiology of irritable bowel syndrome. The research includes basic science and physiology, as well as clinical and translational research.
Our research established the concept of small intestinal bacterial overgrowth as a potential cause of irritable bowel syndrome. This has included the discovery that methane-producing bacteria in the gut can cause constipation. Our work also suggests that pathogenic bacteria impact the intestine via a molecular mimicry mechanism.