Abstract

Ileal pouch-anal anastomosis is the standard surgical treatment for patients with refractory Ulcerative Colitis (UC). However, pouchitis occurs in roughly 50% of UC patients post-pouch creation, despite no previous small bowel inflammation. We hypothesize that pouchitis develops as a result of an abnormal intestinal response to bacterial stasis in a genetically susceptible host. As bacteria are present for a greater duration in stasis, we evaluated the expression of specific toll-like receptors (TLRs), which are major mechanisms for epithelial cells to sense bacteria.

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