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首页> 外文期刊>Infection and immunity >Staphylococcal Esx Proteins Modulate Apoptosis and Release of Intracellular Staphylococcus aureus during Infection in Epithelial Cells
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Staphylococcal Esx Proteins Modulate Apoptosis and Release of Intracellular Staphylococcus aureus during Infection in Epithelial Cells

机译：葡萄球菌的Esx蛋白调节上皮细胞感染过程中细胞凋亡和细胞内金黄色葡萄球菌的释放。

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The opportunistic pathogen Staphylococcus aureus is one of the major causes of health care-associated infections. S. aureus is primarily an extracellular pathogen, but it was recently reported to invade and replicate in several host cell types. The ability of S. aureus to persist within cells has been implicated in resistance to antimicrobials and recurrent infections. However, few staphylococcal proteins that mediate intracellular survival have been identified. Here we examine if EsxA and EsxB, substrates of the ESAT-6-like secretion system (Ess), are important during intracellular S. aureus infection. The Esx proteins are required for staphylococcal virulence, but their functions during infection are unclear. While isogenic S. aureus esxA and esxB mutants were not defective for epithelial cell invasion in vitro, a significant increase in early/late apoptosis was observed in esxA mutant-infected cells compared to wild-type-infected cells. Impeding secretion of EsxA by deleting C-terminal residues of the protein also resulted in a significant increase of epithelial cell apoptosis. Furthermore, cells transfected with esxA showed an increased protection from apoptotic cell death. A double mutant lacking both EsxA and EsxB also induced increased apoptosis but, remarkably, was unable to escape from cells as efficiently as the single mutants or the wild type. Thus, using in vitro models of intracellular staphylococcal infection, we demonstrate that EsxA interferes with host cell apoptotic pathways and, together with EsxB, mediates the release of S. aureus from the host cell.
机译：机会病原体金黄色葡萄球菌是与卫生保健相关的感染的主要原因之一。金黄色葡萄球菌主要是一种细胞外病原体，但是最近有报道称它可以在几种宿主细胞类型中侵袭和复制。金黄色葡萄球菌在细胞内持续存在的能力与抗微生物药和反复感染有关。然而，已鉴定出很少介导细胞内存活的葡萄球菌蛋白。在这里，我们检查ESAT-6样分泌系统（Ess）的底物EsxA和EsxB在细胞内金黄色葡萄球菌感染期间是否重要。 Esx蛋白是葡萄球菌毒力所必需的，但在感染过程中其功能尚不清楚。尽管同基因金黄色葡萄球菌esxA和esxB突变体在体外上皮细胞入侵方面没有缺陷，但与野生型感染的细胞相比，在esxA突变体感染的细胞中观察到早期/晚期凋亡显着增加。通过删除蛋白质的C端残基来阻止EsxA的分泌也导致上皮细胞凋亡的显着增加。此外，用esxA转染的细胞显示出对凋亡细胞死亡的增强保护。同时缺少EsxA和EsxB的双突变体也诱导了细胞凋亡的增加，但值得注意的是，它不能像单突变体或野生型一样有效地从细胞中逃逸。因此，使用细胞内葡萄球菌感染的体外模型，我们证明EsxA干扰宿主细胞的凋亡途径，并与EsxB一起介导金黄色葡萄球菌从宿​​主细胞的释放。

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