Localized colonic inflammation increases cytokine levels in distant small intestinal segments in the rat
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- 作者：Kassem A. Barada ; Fadi H. Mourad ; Sarah I. Sawah ; Carmen Khoury ; Bared Safieh-Garabedian ; Camille F. Nassar and Nayef E. Saadé
- 关键词：Interleukin one ; Interleukin six ; Iodoacetamide ; 2 ; 4 ; 6-trinitrobenzene sulfonic acid
- 刊名：Life Sciences
- 出版年：2006
- 出版时间：19 October 2006
- 年：2006
- 卷：79
- 期：21
- 页码：2032-2042
- 全文大小：1234 K
文摘
Local inflammation in the colon has been associated with nutrient malabsorption and altered motility in the small bowel. These remote effects suggest the release of mediators which can act (or alter) the function of intestinal segments located far from the primary area of inflammation. This study describes the changes in the expression of pro-inflammatory cytokines in the colon and in various segments of the small intestine in two rat models of experimental colitis. Colitis was induced by the intracolonic administration of 100 μL of 6 % iodoacetamide or 250 μL of 2, 4, 6-trinitrobenzene sulfonic acid. Levels of interleukin one beta, interleukin 6, and tumor necrosis factor alpha were measured by ELISA in tissue homogenate sampled from duodenum, jejunum, ileum and colon at different time intervals. In homogenates of strips isolated from duodenum, jejunum and ileum, tumor necrosis alpha and interleukin-6, increased significantly 3–6 h after iodoacetamide or TNBS administration and remained elevated until the colonic inflammation subsided. Interleukin one beta showed comparable but delayed increase. Similar, but more pronounced increase of the three cytokines was noticed in areas of the colon adjacent to the ulcer. Histologic examinations revealed important inflammatory changes in the colon; however, examination of sections from the small intestines did not reveal significant differences between controls and rats with colitis. In conclusion, expression of pro-inflammatory cytokines is increased in remote segments of the small intestines during colitis. The findings may provide a partial explanation or a molecular substrate for the associated small bowel dysfunction.