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Urocortin 1 in Colonic Mucosa in Patients with Ulcerative Colitis

Departments of Pathology (M.S., T.S., H.S.) and Molecular Biology and Applied Physiology (K.T.), Tohoku University School of Medicine, Sendai, Miyagi 980-8575, Japan; and Division of Gastroenterology and Hepatology, Departments of Internal Medicine (M.S., A.T.), and Pathology, Clinical Service (M.K.), Jikei University School of Medicine, Tokyo 105-8461, Japan

Address all correspondence and requests for reprints to: Masayuki Saruta, M.D., Department of Pathology, Tohoku University School of Medicine, 2-1, Seiryo-machi, Aoba-ku, Sendai, Miyagi 980-8575, Japan. E-mail: m-saruta{at}pg7.so-net.ne.jp.

Ulcerative colitis (UC) is characterized by a long-standing chronic inflammation of the bowel with intermittent periods of exacerbation and remission. Its acute exacerbation appears to be related to various stresses. Urocortin 1 (Ucn1) may play important roles in integrated local responses to stress. We therefore examined local production of Ucn1 in patients with UC by immunohistochemistry and mRNA in situ hybridization. Ucn1 immunoreactivity was predominantly detected in lamina propria plasma cells and enterochromaffin cells. In UC patients without glucocorticoid treatment, Ucn1-positive cells and plasma cells increased in proportion to the severity of inflammation (P < 0.0001). Ucn1-positive cells significantly increased in UC patients with advanced inflammatory grades, compared with a control group (P < 0.0001) and nonspecific colitis group (P < 0.0001). In glucocorticoid-treated patients, Ucn1-positive cells were significantly lower in number, compared with the nonglucocorticoid-treated group. Ucn1 mRNA was expressed in lamina propria plasma cells, and both corticotropin-releasing factor₁ and corticotropin-releasing factor_2(a) mRNAs were also partially coexpressed in these cells and macrophages. The present study showed that Ucn1-positive cells were correlated with the severity of inflammation in colonic mucosa with UC, and glucocorticoid treatment decreased these cells. Ucn1 therefore may act as a possible local immune-inflammatory mediator in UC.

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