Sigal Michael, Meyer Thomas F
Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.
Dig Dis. 2016;34(3):190-3. doi: 10.1159/000443349. Epub 2016 Mar 30.
The composition and spatial distribution of our gut microbiota is tightly controlled by the host to prevent bacterial invasion and systemic infection. The gastrointestinal epithelium is predominantly made up of a cellular monolayer equipped with a number of sophisticated autonomous defense mechanisms, which are strikingly efficient in maintaining homeostasis between the luminal microbes and the host. This short review highlights aspects of this finetuned interplay. We also address how deficiencies in mucosal defense can promote disease. First, genetic defects of sensors or effectors of epithelial defense can result in the disruption of the mucosal barrier and lead to chronic inflammatory conditions. Second, chronic colonizers of the gastrointestinal tract can actively manipulate mucosal defense to escape immune surveillance. As shown for Helicobacter pylori in the stomach, sustained manipulation of the epithelium through specialized virulence determinants can increase the risk for genetic lesions and malignant transformation.
宿主严格控制我们肠道微生物群的组成和空间分布,以防止细菌入侵和全身感染。胃肠道上皮主要由一层细胞组成,配备有许多复杂的自主防御机制,这些机制在维持管腔微生物与宿主之间的稳态方面非常有效。这篇简短的综述强调了这种微调相互作用的各个方面。我们还讨论了黏膜防御缺陷如何促进疾病。首先,上皮防御传感器或效应器的遗传缺陷可导致黏膜屏障破坏,并引发慢性炎症状态。其次,胃肠道的慢性定植菌可积极操纵黏膜防御以逃避免疫监视。如在胃中幽门螺杆菌的情况所示,通过特定毒力决定因素持续操纵上皮可增加遗传损伤和恶性转化的风险。