Intestinal inflammation seems invariably to be associated with increased epithelial proliferation. In the small bowel the pathological consequences of this area an increase in the crypt proliferative compartment and a decrease in the absorptive villus compartment, which can lead to malabsorption. In the colon, it is more difficult to examine changes in cell proliferation, but using Ki67, epithelial proliferation has been shown to be increased in ulcerative colitis and parasitic infection. The teleological advantage of increasing epithelial proliferation during intestinal inflammation is presumably in an effort to get rid of parasitized or infected epithelial cells, or to rapidly replace cells which have been lost. Rejection of helminth parasites from rodent small bowel is associated with partial villous atrophy and crypt hypertrophy, which is probably part of the host response making the mucosa inhospitable to the parasites. The short-term nutritional disadvantage of malabsorption is outweighed by the long-term advantage of being parasite-free. However, when the intestinal inflammation is elicited by a dietary constituent, the consequences are only pathological. At the moment there is no information as to the mechanisms by which inflammatory cells alter mucosal morphology and epithelial renewal. The restructuring of mucosal morphology in the flat-mucosa involves considerable adaptation of the connective tissue elements of the lamina propria. Whether this occurs in response to changes in epithelial renewal is not known. Finally, it is clear that activated T cells in the lamina propria can produce a flat-mucosa. In diseases such as Trichuris dysentery and ulcerative colitis there is no or very little T cell activation, even though epithelial proliferation is increased. Increased epithelial proliferation therefore may occur in response to different inflammatory stimuli.