Abstract
A growing body of evidence supports the role of toll-like receptor (TLR) signaling in the intestinal mucosa and its role in inflammation and tumorigenesis. Patients with chronic intestinal inflammation, as is the case with inflammatory bowel disease (IBD), and a subset of patients with inflammatory and sporadic colorectal neoplasia, have increased expression of TLRs, especially TLR4, on colonic epithelial cells. Mouse models of colitis and cancer are useful to understand the role of TLRs and bacteria in the development of colon cancer. Clear differences in bacterial colonization patterns are noted between normal and dysplastic colonic mucosa. TLRs offer a potential prognostic and therapeutic target, serving as the link between bacterial ligands and epithelial inflammation.