Molecular mechanisms of gastric epithelial cell adhesion and injection of CagA by Helicobacter pylori.
Molecular mechanisms of gastric epithelial cell adhesion and injection of CagA by Helicobacter pylori.
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幽门螺杆菌胃上皮细胞粘附和 CagA 注射的分子机制。
DOI：
10.1186/1478-811x-9-28
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发表时间：
2011-11-01
期刊：
影响因子：
--
通讯作者：
Tegtmeyer N
中科院分区：
文献类型：
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作者：
Backert S;Clyne M;Tegtmeyer N
幽门螺杆菌是一种非常成功的病原体，其独特的适应性使其能够在人类中定植。这种细菌的胃感染可引起从慢性胃炎、消化性溃疡到胃癌的病理变化。毒性更强的H.幽门螺杆菌分离物具有许多众所周知的粘附素（BabA/B、SabA、AlpA/B、OipA和HopZ）和编码IV型分泌系统（T4 SS）的cag（细胞毒素相关基因）致病岛。粘附素与宿主靶细胞建立紧密的细菌接触，并且T4 SS代表用于将效应蛋白递送到宿主靶细胞如CagA中的针状菌毛装置。BabA和SabA分别与血型抗原和唾液酸化蛋白结合，并且一系列T4 SS组分包括CagI、CagL、CagY和CagA已被证明靶向整合素β1受体，随后将CagA注射穿过宿主细胞膜。CagA与膜锚定磷脂酰丝氨酸的相互作用也可能在递送过程中发挥作用。虽然我们目前对上述许多因素的理解已经取得了实质性进展，但感染期间OipA、HopZ和AlpA/B的宿主细胞受体仍然是未知的。在这里，我们回顾了最近的进展，表征各种粘附素和结构T4 SS蛋白与宿主细胞因子的相互作用。这些相互作用对H.幽门螺杆菌定植和发病机制进行了讨论。
Helicobacter pylori is a highly successful pathogen uniquely adapted to colonize humans. Gastric infections with this bacterium can induce pathology ranging from chronic gastritis and peptic ulcers to gastric cancer. More virulent H. pylori isolates harbour numerous well-known adhesins (BabA/B, SabA, AlpA/B, OipA and HopZ) and the cag (cytotoxin-associated genes) pathogenicity island encoding a type IV secretion system (T4SS). The adhesins establish tight bacterial contact with host target cells and the T4SS represents a needle-like pilus device for the delivery of effector proteins into host target cells such as CagA. BabA and SabA bind to blood group antigen and sialylated proteins respectively, and a series of T4SS components including CagI, CagL, CagY and CagA have been shown to target the integrin β1 receptor followed by injection of CagA across the host cell membrane. The interaction of CagA with membrane-anchored phosphatidylserine may also play a role in the delivery process. While substantial progress has been made in our current understanding of many of the above factors, the host cell receptors for OipA, HopZ and AlpA/B during infection are still unknown. Here we review the recent progress in characterizing the interactions of the various adhesins and structural T4SS proteins with host cell factors. The contribution of these interactions to H. pylori colonization and pathogenesis is discussed.