Invited Symposium: Arachidonic Acid Metabolites, Other Inflammatory Mediators and Intestinal Ion Transport
The proximity of immune/inflammatory cells to the intestinal epithelium raises the possibility that products of these cells could regulate epithelial transport. Over the past several years, this hypothesis has been amply proven and a variety of cell-cell interactions have been identified that can either up- or down regulate various transport responses. Work from our laboratory has focused on the involvement of mast cells in these processes, although other inflammatory cells can also contribute to these regulatory pathways. Mast cell-derived mediators have been shown to exert both direct and indirect stimulatory effects on epithelial chloride secretion. These effects can be initiated by antigenic stimulation of mast cells, or by agonists not commonly thought of as immune stimuli, such as secretory bile acids. Mast cell mediators, particularly histamine, also appear to regulate duodenal bicarbonate secretion. However, here the effect is inhibitory, and is secondarily mediated by the activation of enteric nerves and possibly by somatostatin. Overall, an understanding of the pathways by which immune/inflammatory mediators regulate the function of the intestinal epithelium may suggest new therapeutic approaches to inflammatory bowel disease, food allergy and peptic ulcer disease, among others.
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|Barrett, KE; (1998). Regulation of Transport by Immune and Inflammatory Mediators. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/rangacharipharm/barrett0846/index.html|
|© 1998 Author(s) Hold Copyright|