Intracellular pathogens need to establish specialised niches for survival and proliferation in host cells. The enteropathogen Salmonella enterica accomplishes this by extensive reorganisation of the host endosomal system deploying the SPI2-encoded type III secretion system (SPI2-T3SS). Fusion events of endosomal compartments with the Salmonella-containing vacuole (SCV) form elaborate membrane networks within host cells enabling intracellular nutrition. However, which host compartments exactly are involved in this process and how the integrity of Salmonella-modified membranes is accomplished are not fully resolved. An RNA interference knockdown screen of host factors involved in cellular logistics identified the ESCRT (endosomal sorting complex required for transport) system as important for proper formation and integrity of the SCV in infected epithelial cells. We demonstrate that subunits of the ESCRT-III complex are specifically recruited to the SCV and membrane network. To investigate the role of ESCRT-III for the intracellular lifestyle of Salmonella, a CHMP3 knockout cell line was generated. Infected CHMP3 knockout cells formed amorphous, bulky SCV. Salmonella within these amorphous SCV were in contact with host cell cytosol, and the attenuation of an SPI2-T3SS-deficient mutant strain was partially abrogated. ESCRT-dependent endolysosomal repair mechanisms have recently been described for other intracellular pathogens, and we hypothesise that minor damages of the SCV during bacterial proliferation are repaired by the action of ESCRT-III recruitment in Salmonella-infected host cells.

中文翻译：

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ESCRT-III复合物在控制含沙门氏菌液泡的完整性中的作用。

细胞内病原体需要建立专门的壁ches，以在宿主细胞中存活和增殖。肠病原肠小肠沙门氏菌通过广泛重组宿主内体系统来实现，该系统采用SPI2编码的III型分泌系统（SPI2-T3SS）。内体区室与含沙门氏菌液泡（SCV）的融合事件在宿主细胞内形成精细的膜网络，从而实现细胞内营养。但是，该过程中确切涉及哪些宿主区室以及沙门氏菌修饰膜的完整性如何实现尚未完全解决。涉及细胞物流的宿主因素的RNA干扰敲低筛选确定ESCRT（运输所需的内体分拣复合体）系统对于在感染的上皮细胞中SCV的正确形成和完整性很重要。我们证明，ESCRT-III复杂的亚基是专门招募到SCV和膜网络。为了研究ESCRT-III在沙门氏菌细胞内生活方式中的作用，产生了CHMP3敲除细胞系。感染的CHMP3基因敲除细胞形成无定形的大体积SCV。这些无定形SCV中的沙门氏菌与宿主细胞胞质溶胶接触，并且部分消除了SPI2-T3SS缺陷型突变株的衰减。最近已对其他细胞内病原体描述了ESCRT依赖性溶酶体修复机制，