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From intestinal stem cells to inflammatory bowel diseases

查看全文 作  者:Michael [1,2]Gersemann;Eduard Friedrich [1,2]Stange;Jan [1,2]Wehkamp 高影响力作者 机构地区:[1]Internal Medicine I,Robert Bosch Hospital,Auerbach-strasse 110,D-70376 Stuttgart, Germany;[2]Dr. Margarete Fischer Bosch Institute of Clinical Pharmacology and University of Tübingen, Auerbachstrasse 112,D-70376 Stuttgart,Germany高影响力机构 出  处:《World Journal of Gastroenterology》索引2011年第17卷第27期,共6页高影响力期刊 基  金:Supported by The Robert Bosch Foundation; Stuttgart; Germany and the Emmy Noether program (Wehkamp J) of the Deutsche Forschungsgemeinschaft (DFG) 摘  要:The pathogenesis of both entities of inflammatory bowel disease (IBD), namely Crohn's disease (CD) and ulcerative colitis (UC), is still complex and under investigation. The importance of the microbial flora in developing IBD is beyond debate. In the last few years, the focus has changed from adaptive towards innate immunity. Crohn's ileitis is associated with a deficiency of the antimicrobial shield, as shown by a reduced expression and secretion of the Paneth cell defensin HD5 and HD6, which is related to a Paneth cell differentiation defect mediated by a diminished expression of the Wnt transcription factor TCF4. In UC, the protective mucus layer, acting as a physical and chemical barrier between the gut epithelium and the luminal microbes, is thin- ner and in part denuded as compared to controls. This could be caused by a missing induction of the goblet cell differentiation factors Hath1 and KLF4 leading to immature goblet cells. This defective Paneth and goblet cell differentiation in Crohn's ileitis and UC may enablethe luminal microbes to invade the mucosa and trigger the inflammation. The exact molecular mechanisms behind ileal CD and also UC must be further clarified, but these observations could give rise to new therapeutic strategies based on a stimulation of the protective innate immune system. 关 键 词:肠道疾病 干细胞 鸡传染性法氏囊病 微生物菌群 溃疡性结肠炎 细胞分化 杯状细胞 发展中国家
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