Several studies have also indicated that TLR4 is the prime sensor of Gram-negative bacteria-derived LPS in vitro, and that TLR4-mediated signaling overexpression promotes inflammation and intestinal damage in mice with dextran sulfate sodium (DSS)-induced colitis (9), whereas TLR4-deficient (TLR4-knockout) mice are protected against this condition (10). Here, TLR4 is linked to colitis.