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The role of interstitial cells of Cajal associated with Auerbach's plexus (ICC-AP) in the pathophysiology of inflammation-induced abnormalities in gut motor activity is poorly understood. Therefore we applied a well-described model of inflammation (infection by Trichinella spiralis) to the mouse small intestine where the structure and function of ICC-AP are best known. Electron microscopic evaluation revealed that 1 to 3 days after infection, selective and patchy damage to the ICC processes occurred, thereby disrupting contacts between these ICC and smooth muscle cells as well as ICC and nerves, which was associated with disordered electrical activity and abnormal peristalsis. Ten to 15 days after infection, damage to ICC-AP was maximal and now involving the cell body and major processes. Our understanding of the role of interstitial cells of Cajal (ICC) in the pathophysiology of intestinal motor disorders related to inflammation is hampered by our limited knowledge of effects of inflammation on this cell system. Therefore, a well-described model of inflammation (infection with T. spiralis) was applied to the mouse small intestine where the structure and function of ICC are best known.ICC associated with Auerbach's plexus (ICC-AP) in the small intestine perform a pacemaker function for intestinal motor activity.1,2 ICC-AP are associated with slowwave-driven peristalsis, which is prominent during gastric emptying and small bowel transit.3 In fact, normal peristaltic activity in the small bowel after gastric emptying of a liquid was absent in W/W v mutant mice that do not have ICC-AP.3 ICC-AP are characterized by elongated cell bodies with extremely long, thin, ramified cell processes interconnected by close apposition contacts and gap junctions. ICC-AP have many ultrastructural features in common with smooth muscle cells and fibroblasts, but can be identified because of a unique combination of ultrastructural features together with unique structural associations with nerves and smooth muscle cells. 4 -6 ICC harbor the c-Kit protein and can therefore be identified at the light microscopy level using immunohistochemistry with c-Kit antibodies. 2,7 In fact, almost all current studies on the pathology of ICC are performed by immunostaining. 8,9 By using both electron microscopy (EM) and immunohistochemistry we discovered in the present study that marked changes in ICC at the EM level, associated with previously observed functional changes, 10 did not lead to any changes at the light microscopy level using Kit immunohistochemistry.

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