Role of IL-10 in Hepatocyte Tight Junction Alteration in Mouse Model of Experimental Colitis

摘要: A variety of hepatobiliary abnormalities have been described in patients with chronic inflammatory bowel diseases (IBDs). The purpose this study was to investigate the role endogenous IL-10 alteration hepatocyte TJ paracellular barrier and rapid transcytotic vesicular pathway modification associated intestinal inflammation. To address question, we used an experimental model colitis, induced by dinitrobenzene sulfonic acid (DNBS). When compared DNBS-treated wild-type (IL-10WT) mice, knock-out mice (IL-10KO) experienced a higher rate extent severity histological signs colon injury. Colon liver levels pro-inflammatory cytokines tumour necrosis factor, interleukin-1β interleukin-6 were also greatly enhanced IL-10KO comparison mice. Liver histology from IL-10WT did not show any parenchymal portal tract inflammation at 4 days after DNBS administration. Serum total bilirubin Alanine aminotransferase, significantly increased DNBS-IL-10KO vs. Therefore, found increase tight junctional permeability lanthanum nitrate (molecular weight, 433) livers mice; accumulated throughout area up most apical region bordering lumen. Absence functional gene resulted significant augmentation diffusion DNBS-induced colitis. Immunofluorescent labelling frozen sections DNBS-IL10KO immunolocalization for claudin-1 ZO-1 localization immunosignals administration DNBS-IL10WT. In conclusion, suggest that absence may represent important pathophysiological mechanism injuries cholestasis observed IBD.