Host Pathogens Molecular Biology Group, Department of Biochemistry and Molecular Biology, Monash University, Clayton VIC, Australia.
Front Cell Infect Microbiol. 2012 Jul 12;2:92. doi: 10.3389/fcimb.2012.00092. eCollection 2012.
More than 50% of the world's population is infected with Helicobacter pylori (H. pylori). Chronic infection with this Gram-negative pathogen is associated with the development of peptic ulcers and is linked to an increased risk of gastric cancer. H. pylori secretes many proteinaceous factors that are important for initial colonization and subsequent persistence in the host stomach. One of the major protein toxins secreted by H. pylori is the Vacuolating cytotoxin A (VacA). After secretion from the bacteria via a type V autotransport secretion system, the 88 kDa VacA toxin (comprised of the p33 and p55 subunits) binds to host cells and is internalized, causing severe "vacuolation" characterized by the accumulation of large vesicles that possess hallmarks of both late endosomes and early lysosomes. The development of "vacuoles" has been attributed to the formation of VacA anion-selective channels in membranes. Apart from its vacuolating effects, it has recently become clear that VacA also directly affects mitochondrial function. Earlier studies suggested that the p33 subunit, but not the p55 subunit of VacA, could enter mitochondria to modulate organelle function. This raised the possibility that a mechanism separate from pore formation may be responsible for the effects of VacA on mitochondria, as crystallography studies and structural modeling predict that both subunits are required for a physiologically stable pore. It has also been suggested that the mitochondrial effects observed are due to indirect effects on pro-apoptotic proteins and direct effects on mitochondrial morphology-related processes. Other studies have shown that both the p55 and p33 subunits can indeed be efficiently imported into mammalian-derived mitochondria raising the possibility that they could re-assemble to form a pore. Our review summarizes and consolidates the recent advances in VacA toxin research, with focus on the outstanding controversies in the field and the key remaining questions that need to be addressed.
世界上超过 50%的人口感染了幽门螺杆菌(H. pylori)。这种革兰氏阴性病原体的慢性感染与消化性溃疡的发展有关,并与胃癌风险增加有关。H. pylori 分泌许多对初始定植和随后在宿主胃中持续存在很重要的蛋白质因子。H. pylori 分泌的主要蛋白毒素之一是空泡细胞毒素 A(VacA)。这种 88 kDa 的 VacA 毒素(由 p33 和 p55 亚基组成)在通过 V 型自转运分泌系统从细菌中分泌后,与宿主细胞结合并被内化,导致严重的“空泡化”,其特征是大泡的积累,这些大泡既有晚期内体的特征,也有早期溶酶体的特征。“空泡”的形成归因于 VacA 在膜中形成阴离子选择性通道。除了其空泡化作用外,最近清楚的是,VacA 还直接影响线粒体功能。早期的研究表明,VacA 的 p33 亚基,而不是 p55 亚基,可以进入线粒体来调节细胞器功能。这就提出了一种可能性,即除了形成孔之外,还有一种单独的机制可能负责 VacA 对线粒体的作用,因为晶体学研究和结构建模预测两个亚基都是形成生理稳定孔所必需的。也有人认为,观察到的线粒体效应是由于对促凋亡蛋白的间接影响和对与线粒体形态相关的过程的直接影响。其他研究表明,p55 和 p33 亚基实际上都可以有效地被导入哺乳动物衍生的线粒体中,这增加了它们可以重新组装形成孔的可能性。我们的综述总结并整合了 VacA 毒素研究的最新进展,重点介绍了该领域的突出争议和需要解决的关键遗留问题。