External membrane vesicles from Helicobacter pylori induce apoptosis in gastric epithelial cells
External membrane vesicles from Helicobacter pylori induce apoptosis in gastric epithelial cells
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DOI：
10.1111/j.1574-6968.2006.00305.x
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发表时间：
2006-07-01
影响因子：
2.1
通讯作者：
Melendez-Zajgla, Jorge
中科院分区：
文献类型：
--
作者：
Ayala, Guadalupe;Torres, Luz;Melendez-Zajgla, Jorge
胃粘膜幽门螺杆菌感染是最常见的感染性疾病之一，与消化性溃疡和胃癌等多种临床结局相关。幽门螺杆菌引起的胃粘膜细胞损伤受细菌毒力因子控制，包括VacA和CagA。外膜囊泡不断脱落的细菌，并可以提供一个额外的机制，致病性释放非分泌因子，然后可以与上皮细胞相互作用。本报告显示，外膜囊泡能够诱导胃（AGS）上皮细胞的线粒体途径不介导的细胞凋亡，如通过缺乏细胞色素c释放与半胱天冬酶8和3的激活所证明的。由这些囊泡诱导的细胞凋亡不需要经典的VacA（+）表型，因为具有截短的并且因此非分泌形式的该蛋白的阴性菌株也可以诱导细胞死亡。这些结果在今后的H.幽门螺杆菌菌株的致病性明显为VacA-。
The Helicobacter pylori infection of gastric mucosa is one of the most common infectious diseases and is associated with a variety of clinical outcomes, including peptic ulcer disease and gastric cancer. Helicobacter pylori-induced damage to gastric mucosal cells is controlled by bacterial virulence factors, which include VacA and CagA. Outer membrane vesicles are constantly shed by the bacteria and can provide an additional mechanism for pathogenicity by releasing non-secretable factors which can then interact with epithelial cells. The present report shows that external membrane vesicles are able to induce apoptosis not mediated by mitochondrial pathway in gastric (AGS) epithelial cells, as demonstrated by the lack of cytochrome c release with an activation of caspase 8 and 3. Apoptosis induced by these vesicles does not require a classic VacA(+) phenotype, as a negative strain with a truncated and therefore non-secretable form of this protein can also induce cell death. These results should be taken into account in future studies of H. pylori pathogenicity in strains apparently VacA-.