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首页> 外文期刊>Journal of bacteriology >EssE Promotes Staphylococcus aureus ESS-Dependent Protein Secretion To Modify Host Immune Responses during Infection
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EssE Promotes Staphylococcus aureus ESS-Dependent Protein Secretion To Modify Host Immune Responses during Infection

机译：EssE促进金黄色葡萄球菌ESS依赖蛋白的分泌，以在感染过程中修改宿主的免疫反应。

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摘要

Staphylococcus aureus, an invasive pathogen of humans and animals, requires a specialized ESS pathway to secrete proteins (EsxA, EsxB, EsxC, and EsxD) during infection. Expression of ess genes is required for S. aureus establishment of persistent abscess lesions following bloodstream infection; however, the mechanisms whereby effectors of the ESS pathway implement their virulence strategies were heretofore not known. Here, we show that EssE forms a complex with other members of the ESS secretion pathway and its substrates, promoting the secretion of EsxA, EsxB, EsxC, EsxD, and EssD. During bloodstream infection of mice, the S. aureus essE mutant displays defects in host cytokine responses, specifically in the production of interleukin-12 (IL-12) (p40/p70) and the suppression of RANTES (CCL5), activators of TH1 T cell responses and immune cell chemotaxis, respectively. Thus, essE-mediated secretion of protein effectors via the ESS pathway may enable S. aureus to manipulate host immune responses by modifying the production of cytokines.
机译：金黄色葡萄球菌是人类和动物的一种侵入性病原体，需要专门的ESS途径在感染过程中分泌蛋白质（EsxA，EsxB，EsxC和EsxD）。 ess 基因的表达对于血流感染后金黄色葡萄球菌持续脓肿病变的建立是必需的;然而，迄今为止尚不清楚ESS途径的效应子实施其毒力策略的机制。在这里，我们显示EssE与ESS分泌途径的其他成员及其底物形成复合物，从而促进EsxA，EsxB，EsxC，EsxD和EssD的分泌。在小鼠的血液感染过程中，金黄色葡萄球菌 essE 突变体在宿主细胞因子反应中显示出缺陷，特别是在白介素12（IL-12）（p40 / p70）的产生和RANTES的抑制（ CCL5），T H 1 T细胞应答激活剂和免疫细胞趋化性。因此，通过ESS途径的 essE 介导的蛋白质效应子的分泌可能使金黄色葡萄球菌能够通过修饰细胞因子的产生来操纵宿主的免疫反应。

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