Backert Steffen, Schmidt Thomas P, Harrer Aileen, Wessler Silja
Division of Microbiology, Department of Biology, Friedrich Alexander University Erlangen-Nuremberg, Staudtstr. 5, 91058, Erlangen, Germany.
Division of Microbiology, Department of Molecular Biology, Paris-Lodron University of Salzburg, Billroth Str. 11, 5020, Salzburg, Austria.
Curr Top Microbiol Immunol. 2017;400:195-226. doi: 10.1007/978-3-319-50520-6_9.
Highly organized intercellular tight and adherens junctions are crucial structural components for establishing and maintenance of epithelial barrier functions, which control the microbiota and protect against intruding pathogens in humans. Alterations in these complexes represent key events in the development and progression of multiple infectious diseases as well as various cancers. The gastric pathogen Helicobacter pylori exerts an amazing set of strategies to manipulate these epithelial cell-to-cell junctions, which are implicated in changing cell polarity, migration and invasive growth as well as pro-inflammatory and proliferative responses. This chapter focuses on the H. pylori pathogenicity factors VacA, CagA, HtrA and urease, and how they can induce host cell signaling involved in altering cell-to-cell permeability. We propose a stepwise model for how H. pylori targets components of tight and adherens junctions in order to disrupt the gastric epithelial cell layer, giving fresh insights into the pathogenesis of this important bacterium.
高度有序的细胞间紧密连接和黏附连接是建立和维持上皮屏障功能的关键结构组成部分，上皮屏障功能可控制微生物群并抵御人类病原体的入侵。这些复合物的改变是多种传染病以及各种癌症发生和发展的关键事件。胃病原体幽门螺杆菌运用一系列惊人的策略来操纵这些上皮细胞间连接，这些连接与细胞极性改变、迁移、侵袭性生长以及促炎和增殖反应有关。本章重点关注幽门螺杆菌的致病因子VacA、CagA、HtrA和脲酶，以及它们如何诱导宿主细胞信号传导，从而改变细胞间通透性。我们提出了一个逐步模型，说明幽门螺杆菌如何靶向紧密连接和黏附连接的成分，以破坏胃上皮细胞层，这为深入了解这种重要细菌的发病机制提供了新的见解。
