| Inflammatory bowel disease (IBD) is a chronic inflammatory disorder but its etiology has not been clearly understood. Immunodysfunction has been considered as the prominent factor in its pathogenesis. Macrophages might play a key role in immunologic mechanism of IBD as abundant inflammatory cells infiltrating from patients' inlamed gut, including macrophages and neutrophils. Gastrointestinal mucosa is endowed with several antioxidant defense systems, including the reduced glutathione (GSH) focusing on neutralizing the damaging effects of ROS. GSH plays a major role in gastrointestinal mucosal cytoprotection against oxidative stress in a variety of models. Indeed, previous studies examing the status of antioxidants in mucosa from IBD patients and experimental animal models of colitis have reported a decrease in the level of antioxidants, including that of GSH.According to Murata Y at el , macrophages can be divided into two classes basing on intracellular GSH level, namely the reductive macrophages (RMp) with high expression of intracellular concent of GSH and the oxidative macrophages (OMp) with less content of GSH. Several other studies reported that Crohn' disease (CD) is classified as RMp/Th1 type response but OMp/Th2 type is associated with inflammatory cells infiltration. However, it isn't clearly known about the transformation of GSH of local colon and immune cells in Dextran Sodium Sulphate (DSS) induced colitis and its relationships with mucosal injury and cytokine profile. In this study, we explore the expression of reduced glutathion (GSH) of colonic mucosa and GSH/GSSG within celiac macrophages in DSS-induced acute colitis and the relationship between GSH transformation and Th1/Th2 cytokine profile- IL-4 and IFN-γ as well as mucosal injury. Inaddition, to explore the role of macrophages in the pathogenesis and development of this type of colitis.1.Characteristics of Glutathion of inflamed colon in Dextran Sodium Sulphate induced acute colitis of mice and its relationships with mucosal injury and production of IFN-γand IL-4 .Methods BALB/C mice were fed with 5% DSS for 7days to induce acute experimental colitis, the colonic mucosa were checked histopathologically and GSH expression was evaluated with GSH1 Ab ; the expression of IL-4 and IFN-γ was also analyzed with ELISA. Results acute colitis was confirmed histopathologically in DSS group characterized by focal crypt lesions with granulocytes and macrophages in mucosa and submucosa. The level of GSH in DSS group was downregulated compared with that of control group. An increased IL-4 and a decreased IFN-γ were noticed. Conclusion Low expression of GSH is related with the increased IL-4 /decreased IFN-γ as well as mucosal injury in DSS-induced acute colitis of mice.2.The relationship of GSH/GSSG within celiac macrophages with mucosal injury and cytokine profile- IL-4 and IFN-γ in Dextran Sodium Sulphate-induced acute colitis of miceMethods BALB/C mice were fed with 5% DSS for 7days to induce experimental colitis, and macrophages in abdominal cavity were collected, the GSH, GSSG and GSH/GSSG in celiac macrophages were determined by Glutathione Assay Kits. The colon was isolated for both histopathological study and evaluation of IL-4 and IFN-γ as well as GSH expression. Results. The expression of GSH in celiac macrophages was downregulated but GSSG upregulated in DSS group, therefore the ratio of GSH/GSSG decreased significantly compared with that of control group. A notable increase of IL-4 in colon and a decrease of IFN-y in spleen were noticed in the DSS-induced colitis .Conclusion The type of celiac macrophages in DSS-induced colitis was...
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