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1 Department of Biomedical Sciences, Creighton University School of Medicine, Omaha 68178; and 2 Department of Veterans Affairs Medical Center, Omaha, Nebraska 68105
Our aim was to investigate the cause-effect relationship between intestinal inflammation induced by infection with enteric stages of Trichinella spiralis and decreased host food intake. A suppression of food intake in T. spiralis-infected rats occurred within the first 24 h postinfection (PI) and was maximized by day 6 PI. Food intake, cumulated over an 8-day PI period, decreased by 59% compared with uninfected animals. The anti-inflammatory glucocorticoid betamethasone 21-phosphate was orally administered to rats in their drinking water to suppress T. spiralis-induced jejunal inflammation. When treated with a low dose of glucocorticoid (5.2 µg/ml), food intake in infected rats was still significantly reduced, but only by 21% compared with glucocorticoid-treated, uninfected rats. At the highest glucocorticoid dose (10.4 µg/ml) administered, infection-induced reduction in food intake was not different from that of glucocorticoid-treated, uninfected counterparts. The elevation in jejunal myeloperoxidase activity caused by infection was also significantly blunted by oral glucocorticoid treatment. Our results suggest that suppressed host food intake during enteric T. spiralis infection is directly linked to intestinal inflammation.
feeding behavior; Trichinella spiralis; betamethasone 21-phosphate; anti-inflammatory glucocorticoid; mucosal inflammation; small intestine; myeloperoxidase activity
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J R McDermott, F C Leslie, M D'Amato, D G Thompson, R K Grencis, and J T McLaughlin Immune control of food intake: enteroendocrine cells are regulated by CD4+ T lymphocytes during small intestinal inflammation Gut, April 1, 2006; 55(4): 492 - 497. [Abstract] [Full Text] [PDF] |
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