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NEUROREGULATION AND MOTILITY

IL-1 inhibits intestinal smooth muscle proliferation in an organ culture system: involvement of COX-2 and iNOS induction in muscularis resident macrophages

¹Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Tokyo, Japan; ²Paratuberculosis and Inflammatory Bowel Disease Research Team, National Institute of Animal Health, Tsukuba, Japan; and ³Department of Pharmacology, University of Nevada School of Medicine, Reno, Nevada

Submitted 20 October 2006 ; accepted in final form 17 January 2007

Intestinal inflammation causes hyperplasia of smooth muscle that leads to thickening of the smooth muscle layer, resulting in dysmotility. IL-1 is a proinflammatory cytokine that plays a central role in intestinal inflammation. In this study, to evaluate the effect of IL-1 on proliferation of ileal smooth muscle cells in vivo, we utilized an organ culture system. When rat ileal smooth muscle tissue was cultured under serum-free conditions for 3 days, most smooth muscle cells maintained their arrangement and kept their contractile phenotype. When 10% FBS was added, an increased number of smooth muscle cells per unit area was observed. Moreover, immunohistochemical staining for PCNA demonstrated that FBS induced proliferation of smooth muscle cells. IL-1 inhibited the proliferative effect of FBS. Furthermore, IL-1 upregulated inducible nitric oxide (NO) synthase and cyclooxygenase-2 mRNA and protein and thus stimulated NO and PGE₂ productions. Moreover, exogenously applied NO and PGE₂ inhibited the increase of bromodeoxyuridine-positive cells stimulated with FBS. Immunostaining revealed that the majority of cyclooxygenase-2 and inducible NO synthase was located in the dense network of macrophages resident in the muscularis, which were immunoreactive to ED2. Based on these findings, IL-1 acts as an anti-proliferative mediator, which acts indirectly through the production of PGE₂ and NO from resident macrophage within ileal smooth muscle tissue.

interleukin-1; intestine

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