Pathophysiology of disrupted intestinal mucosal barrier (increased permeability and protein loss)

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1.Intestinal permeabilityOleic acid and taurocholate, both post prandial intestinal contents, could increase the intestinal permeability in a dose dependent manner. The mucus gellayr inhibited the increased permeability induced by intraluminal factors, and this action may contribute to the intestinal mucosal barrier function. Intestinal mucosal permeability is also increased by not only exogenously administered nitric oxide (NO) but also by NO produced by intestinal epithelial cells.2.Chemokine production by intestinal epithelial cellThe produstion of interleukin (IL) -8 by intestinal epithelial cells was increased in the presence of IL-1 beta or TNFalpha. Cyclosporine A significantly reduced cytokine induced IL-8 production, whereas FK506 or dexamethasone had no effect. The production of MCP-1 and eotaxin were also increased by intestinal epithelial cells in the presence of IL-1 beta or TNFalpha. Sodium butyrate, a short-chain fatty acid, reduced cytokine-induced these chemokine production.3.Fecal proteins in patients with inflammatory bowel disease (IBD)The fecal levels of neutrophil-derived proteins were increased in patients with inflammatory bowel disease. Lf was the most suitable of these proteins to use as a neutrophil-derived fecal marker of inflammation for clinical application. An increase of fecal alpha1-antitrypsin (AT) level is at least partly due to an increase of its secretion from intestinal epithelial cells in patients with intestinal inflammation. The structural analysis of fecal alpha1-AT is useful for assessment of disease activity in IBD.The measurement of eosinophil granule-derived proteins in feces is useful for monitoring the disease activity and predicting relapse in patients with IBD.Eosinophil protein X (EPX,EDN) may be more suit able than eosinophil cationic protein (ECP) as a fecal eosinophil marker.