首页> 外文期刊>Zeitschrift fur Gastroenterologie >Mucosal protection by phosphatidylcholine as new therapeutic concept in ulcerative colitis [Mukosaschutz durch Phosphatidylcholin als neues therapeutisches Prinzip bei der Colitis ulcerosa]
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Mucosal protection by phosphatidylcholine as new therapeutic concept in ulcerative colitis [Mukosaschutz durch Phosphatidylcholin als neues therapeutisches Prinzip bei der Colitis ulcerosa]

机译:磷脂酰胆碱的粘膜保护作为溃疡性结肠炎的一种新治疗方法[溃疡性结肠炎的粘膜保护作为溃疡性结肠炎的一种新治疗原理]

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摘要

The colonic mucus serves a first barrier towards invasion of commensal bacteria in stool. One essential component of intestinal mucus is phosphatidylcholine (PC) which represents more than 90 % of the phospholipids in mucus indicative for a selective transport of PC into this compartment. It is arranged in lamellar structures as surfactant-like particles which provide a hydrophobic surface on top of the hydrated mucus gel to prevent invasion of bacteria from the intestinal lumen. In ulcerative colitis (UC) the mucus PC content is reduced by 70 % irrespective of the state of inflammation. Thus, it could represent an intrinsic primary pathogenetic condition predisposing to bacterial invasion and precipitation of inflammation. Since PC was shown to be mainly secreted by the ileal mucosa from where it is assumed to move distally to the colon, the PC content along the colonic wall towards the rectum gradually thins out with lowest PC content in the rectum. It explains the start of the clinical manifestation of UC in the rectum and expansion from there to the upper parts of the colon. When the lacking mucus PC in the UC was supplemented by an oral, delayed released PC preparation, it was shown in three clinical trials that the inflammation improved and even resolved. The data indicate the essential role of the mucus phosphatidylcholine content for protection against inflammation in colon. This can be the basis for the development of an innovative therapy for ulcerative colitis using orally available delayed released phosphatidylcholine.
机译:结肠粘液是粪便中共生细菌入侵的第一道屏障。肠粘液的一种基本成分是磷脂酰胆碱(PC),它代表粘液中90%以上的磷脂,表明PC选择性转运入该区室。它以表面活性剂样颗粒的层状结构排列,在水合粘液凝胶的顶部提供疏水表面,以防止细菌从肠腔侵入。在溃疡性结肠炎(UC)中,无论炎症状态如何,粘液PC含量都会减少70%。因此,它可能代表了固有的主要致病条件,容易引起细菌入侵和炎症沉淀。由于显示PC主要是由回肠粘膜分泌的,因此假定PC从那里向远端移动至结肠,因此沿结肠壁朝向直肠的PC含量逐渐变薄,直肠中PC含量最低。它解释了UC在直肠中的临床表现的开始以及从那里到结肠上部的扩张。当通过口服,延迟释放的PC制剂补充UC中缺乏黏液的PC时,在三项临床试验中表明炎症得到改善甚至消失。数据表明粘液磷脂酰胆碱含量对于保护结肠免于炎症起着至关重要的作用。这可以作为开发口服溃疡延迟性磷脂酰胆碱用于溃疡性结肠炎的创新疗法的基础。

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