Pathogenesis of Helicobacter pylori infection
Pathogenesis of Helicobacter pylori infection
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DOI：
10.1111/hel.12335
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发表时间：
2016-09-01
期刊：
影响因子：
4.4
通讯作者：
Naumann, Michael
中科院分区：
文献类型：
--
作者：
Backert, Steffen;Neddermann, Matthias;Naumann, Michael
据估计，幽门螺杆菌感染了世界上一半以上的人口，是慢性胃炎、消化性溃疡疾病、MALT淋巴瘤和胃腺癌的主要危险因素。幽门螺杆菌感染和临床后果是由宿主、定植细菌和环境参数之间高度复杂的相互作用控制的。与胃病发展相关的重要细菌决定因素包括编码IV型分泌系统（T4SS）的cag致病性岛、易位效应蛋白CagA、空泡化细胞毒素VacA、粘附素BabA、脲酶、丝氨酸蛋白酶HtrA、分泌的外膜囊泡等。大量的这些因素和相应基因的等位基因变化揭示了一个复杂的图景和评估每个不同组成部分的影响的问题。已经开展了大量的工作，以确定与幽门螺杆菌引发的发病机制相关的分子过程，使用蒙古沙鼠、小鼠、原代组织以及新的体外模型系统，如胃。细菌对宿主信号级联的操纵似乎对诱导致病性下游活动和胃病进展至关重要。在这里，我们回顾了这一重要研究领域的最新进展。
Helicobacter pylori is estimated to infect more than half of the worlds human population and represents a major risk factor for chronic gastritis, peptic ulcer disease, MALT lymphoma, and gastric adenocarcinoma. H.pylori infection and clinical consequences are controlled by highly complex interactions between the host, colonizing bacteria, and environmental parameters. Important bacterial determinants linked with gastric disease development include the cag pathogenicity island encoding a type IV secretion system (T4SS), the translocated effector protein CagA, vacuolating cytotoxin VacA, adhesin BabA, urease, serine protease HtrA, secreted outer membrane vesicles, and many others. The high quantity of these factors and allelic changes in the corresponding genes reveals a sophisticated picture and problems in evaluating the impact of each distinct component. Extensive work has been performed to pinpoint molecular processes related to H.pylori-triggered pathogenesis using Mongolian gerbils, mice, primary tissues, as well as novel in vitro model systems such as gastroids. The manipulation of host signaling cascades by the bacterium appears to be crucial for inducing pathogenic downstream activities and gastric disease progression. Here, we review the most recent advances in this important research area.