Epithelial transport and gut barrier function in colitis
Epithelial transport and gut barrier function in colitis
复制标题
DOI：
10.1097/00001574-200311000-00011
复制
发表时间：
2003-11-01
影响因子：
2.5
通讯作者：
Barrett, KE
中科院分区：
文献类型：
--
作者：
McCole, DF;Barrett, KE
综述目的结肠炎是一种局限于结肠的炎症性肠病，其特征是水样腹泻，也可伴有便血。与结肠炎相关的炎症通常局限于粘膜和粘膜下层，尽管克罗恩氏结肠炎可能是透壁的。结肠粘膜的主要功能是作为肠道内腔内容物的屏障，并促进水和电解质的双向运输。已经确定屏障和转运缺陷发生在结肠炎中，并且可能参与发病机制。因此，本文综述了最近的证据，可能涉及在扰动的粘膜转运和屏障功能的结肠炎和治疗进展，以抵消这些缺陷的潜在机制，最近的发现负责结肠炎的转运功能障碍和屏障缺陷的机制进行了讨论，包括运输蛋白的活性降低，如Cl细菌与上皮的相互作用，包括对NOD-2的调节和功能的理解，以及肠屏障成分的表达改变，如粘蛋白和多药耐药蛋白。所讨论的工作还可以确定在结肠炎中功能改变的新靶点，这些靶点可能通过现有药物或正在开发的新药物进行治疗调节。
Purpose of reviewColitis is an inflammatory bowel disease that is confined to the colon and is characterized by a watery diarrhea that can also be accompanied by blood in the stool. The inflammation associated with colitis is generally confined to the mucosal and submucosal layers, although Crohn's colitis may be transmural. The principal functions of the colonic mucosa are to act as a barrier to the luminal contents of the intestinal tract and to facilitate the bidirectional transport of water and electrolytes. It is well established that barrier and transport defects occur in colitis and may be involved in pathogenesis. Consequently, this review discusses recent evidence of potential mechanisms that may be involved in the perturbation of mucosal transport and barrier functions in colitis and therapeutic advances to counteract these defectsRecent findingsMechanisms responsible for transport dysfunction and barrier defects in colitis are discussed, including decreased activity of transport proteins such as Cl bacterial interactions with the epithelium, including understanding of the regulation and function of NOD-2, and altered expression of components of the intestinal barrier, such as mucins and multidrug resistance proteins.SummaryRecent advances in our understanding of how changes in barrier and transport function occur in colitis may illuminate the pathophysiology of this condition. The work discussed may also identify novel targets that are functionally altered in colitis, which potentially can be modulated therapeutically either with existing medications or with newer agents that are in development.