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Intestinal Permeability in Inflammatory Bowel Disease: Pathogenesis Clinical Evaluation and Therapy of Leaky Gut

机译:肠道炎性肠通透性:发病机理临床评估和漏泄肠道治疗。

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摘要

The pathogenesis of inflammatory bowel disease (IBD) is multifactorial with data suggesting the role of a disturbed interaction between the gut and the intestinal microbiota. A defective mucosal barrier may result in increased intestinal permeability which promotes the exposition to luminal content and triggers an immunological response that promotes intestinal inflammation. IBD patients display several defects in the many specialized components of mucosal barrier, from the mucus layer composition to the adhesion molecules that regulate paracellular permeability. These alterations may represent a primary dysfunction in Crohn's disease, but they may also perpetuate chronic mucosal inflammation in ulcerative colitis. In clinical practice, several studies have documented that changes in intestinal permeability can predict IBD course. Functional tests, such as the sugar absorption tests or the novel imaging technique using confocal laser endomicroscopy, allow an in vivo assessment of gut barrier integrity. Antitumor necrosis factor-α (TNF-α) therapy reduces mucosal inflammation and restores intestinal permeability in IBD patients. Butyrate, zinc, and some probiotics also ameliorate mucosal barrier dysfunction but their use is still limited and further studies are needed before considering permeability manipulation as a therapeutic target in IBD.
机译:炎症性肠病(IBD)的发病机制是多因素的,有数据表明肠道和肠道菌群之间相互作用受干扰的作用。有缺陷的粘膜屏障可能会导致肠道通透性增加,从而促进肠腔内物质的暴露,并触发促进肠道炎症的免疫反应。 IBD患者在粘膜屏障的许多特殊成分中显示出一些缺陷,从粘液层组成到调节细胞旁通透性的粘附分子。这些改变可能代表了克罗恩病的原发性功能障碍,但也可能使溃疡性结肠炎的慢性粘膜炎症永久化。在临床实践中,一些研究已经证明肠通透性的变化可以预测IBD病程。功能测试,例如糖吸收测试或使用共聚焦激光内镜的新型成像技术,可在体内评估肠道屏障的完整性。抗肿瘤坏死因子-α(TNF-α)治疗可减轻IBD患者的粘膜炎症并恢复肠道通透性。丁酸盐,锌和一些益生菌也可改善粘膜屏障功能障碍,但其使用仍然受到限制,在将通透性操纵作为IBD的治疗目标之前,还需要进一步研究。

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