Collectively, these results indicate that (i) Muc2 promotes host-mediated colonization resistance when commensals are depleted; and (ii) commensal bacteria, although initially important in promoting colonization resistance in both strains, ultimately come into direct contact with large numbers of PMNs following the infection-induced ulceration that occurs in a Muc2-deficient environment. This evidence concerns the gene MUC2 and infection.