The role of smooth muscle in intestinal inflammation

The observation that active ulcerative colitis is accompanied by a reduction in motor activity in the distal colon1–3 suggests that the contractility of colonic smooth muscle may be impaired as a result of inflammation. this has been confirmed in an in-vitro study of human colonic circular muscle in which contraction induced by either bethanechol or KC1 was significantly reduced in comparison to muscle obtained from patients without inflammatory bowel disease (IBD)4, suggesting that the underlying mechanism is located at the postreceptor level in the excitation—contraction coupling of the muscle cell. Similar observations have been made in animal models of colitis5. In our study5, a similar decrease in colonic smooth muscle contractility was observed in colitis induced by chemical injury (acetic acid or trinitrobenzene sulfonic acid, TNB), as well as infection (Trichinella spiralis) These results also illustrate that inflammation-induced changes in smooth muscle are nonspecific in that they do not appear to be influenced by the manner in which colitis is induced.