Department of Pathology, The University of Chicago, Chicago, IL 60637, USA.
Curr Opin Pharmacol. 2009 Dec;9(6):715-20. doi: 10.1016/j.coph.2009.06.022. Epub 2009 Jul 24.
The intestinal epithelium restricts free passage of toxic and infectious molecules from the gut lumen while allowing selective paracellular absorption across the tight junction. Inflammatory bowel disease (IBD) patients demonstrate a loss of tight junction barrier function, increased pro-inflammatory cytokine production, and immune dysregulation; however, the relationship between these events is incompletely understood. Although tight junction barrier defects are insufficient to cause experimental IBD, mucosal immune activation is altered in response to increased epithelial permeability. Thus, an evolving model suggests that barrier dysfunction may predispose or enhance disease progression and therapies targeted to specifically restore the barrier function may provide an alternative or supplement to immunology-based therapies.
肠道上皮组织限制有毒和传染性分子从肠腔自由通过，同时允许选择性的紧密连接旁细胞吸收。炎症性肠病（IBD）患者表现出紧密连接屏障功能丧失、促炎细胞因子产生增加和免疫失调；然而，这些事件之间的关系尚未完全了解。尽管紧密连接屏障缺陷不足以导致实验性 IBD，但黏膜免疫激活会因上皮通透性增加而发生改变。因此，一个不断发展的模型表明，屏障功能障碍可能导致或增强疾病进展，而专门恢复屏障功能的治疗方法可能为基于免疫学的治疗方法提供替代或补充。
