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TLR signaling at the intestinal epithelial interface

Unlike other epithelial surfaces in the body, the intestinal epithelium is exposed to a high concentration of bacteria and bacterial products. This situation is particularly true in the colon where there is an estimated 10 bacteria per gram of tissue. In spite of the density of commensal bacteria in the colon, the normal intestinal mucosa maintains a controlled state of inflammation characterized by lamina propria lymphocytes, macrophages and dendritic cells in the absence of neutrophils. In patients with idiopathic inflammatory bowel disease, however, the intestinal mucosal immune system generates an overly aggressive immune response in the presence of bacteria resulting in intestinal epithelial cell damage, ulcerations, and diarrhea. A delicate balance exists between the human host and the intestinal microbiota. Understanding this delicate balance may provide clues to situations in which the balance is disturbed such as inflammatory bowel disease. Colonic epithelial cells form a relatively impermeable monolayer held together by tight junctions, occludins junctions and claudins that do not permit the passage of LPS or bacteria. Although an important function of the intestinal epithelium is to form a barrier, the epithelium is also an active participant in the mucosal immune response, especially to pathogenic bacteria, through its secretion of chemokines such as IL-8. In health, the combination of an impermeable epithelial barrier and controlled antigen presentation results in a state of tolerance to autologous commensal flora. By contrast, patients with inflammatory bowel disease are characterized by an abnormal immune response to commensal flora, clinical improvement with diversion of the fecal