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首页> 外文期刊>Infection and immunity >Salmonella enterica Serovar Typhimurium Binds to HeLa Cells via Fim-Mediated Reversible Adhesion and Irreversible Type Three Secretion System 1-Mediated Docking
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Salmonella enterica Serovar Typhimurium Binds to HeLa Cells via Fim-Mediated Reversible Adhesion and Irreversible Type Three Secretion System 1-Mediated Docking

机译：沙门氏菌血清型鼠伤寒沙门氏菌通过Fim介导的可逆粘附和不可逆类型三分泌系统1介导的对接与HeLa细胞结合

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The food-borne pathogen Salmonella enterica serovar Typhimurium invades mammalian epithelial cells. This multistep process comprises bacterial binding to the host cell, activation of the Salmonella type three secretion system 1 (T1), injection of effector proteins, triggering of host cell actin rearrangements, and S. Typhimurium entry. While the latter steps are well understood, much less is known about the initial binding step. Earlier work had implicated adhesins (but not T1) or T1 (but not other adhesins). We have studied here the Salmonella virulence factors mediating S. Typhimurium binding to HeLa cells. Using an automated microscopy assay and isogenic S. Typhimurium mutants, we analyzed the role of T1 and of several known adhesins (Fim, Pef, Lpf, Agf, and Shd) in host cell binding. In wild-type S. Typhimurium, host cell binding was mostly attributable to T1. However, in the absence of T1, Fim (but not Pef, Lpf, Agf, and Shd) also mediated HeLa cell binding. Furthermore, in the absence of T1 and type I fimbriae (Fim), we still observed residual binding, pointing toward at least one additional, unidentified binding mechanism. Dissociation experiments established that T1-mediated binding was irreversible (“docking”), while Fim-mediated binding was reversible (“reversible adhesion”). Finally, we show that noninvasive bacteria docking via T1 or adhering via Fim can efficiently invade HeLa cells, if actin rearrangements are triggered in trans by a wild-type S. Typhimurium helper strain. Our data show that binding to HeLa cells is mediated by at least two different mechanisms and that both can lead to invasion if actin rearrangements are triggered.
机译：食源性病原体肠道沙门氏菌鼠伤寒沙门氏菌侵入哺乳动物上皮细胞。这个多步骤过程包括细菌与宿主细胞的结合，沙门氏菌三型分泌系统1（T1）的激活，效应蛋白的注射，宿主细胞肌动蛋白重排的触发和鼠伤寒沙门氏菌的进入。虽然后面的步骤是很好理解的，但对初始结合步骤的了解却很少。早期的工作涉及粘附素（但不是T1）或T1（但不是其他粘附素）。我们在这里研究了介导鼠伤寒沙门氏菌与HeLa细胞结合的沙门氏菌毒力因子。使用自动显微镜检测和同基因的鼠伤寒沙门氏菌突变体，我们分析了T1和几种已知的粘附素（Fim，Pef，Lpf，Agf和Shd）在宿主细胞结合中的作用。在野生型鼠伤寒沙门氏菌中，宿主细胞的结合主要归因于T1。但是，在没有T1的情况下，Fim（但不是Pef，Lpf，Agf和Shd）也介导HeLa细胞结合。此外，在没有T1和I型菌毛（Fim）的情况下，我们仍然观察到残留的结合，指向至少一种另外的未确定的结合机制。解离实验确定，T1介导的结合是不可逆的（“对接”），而Fim介导的结合是可逆的（“可逆的粘附”）。最后，我们表明，如果野生型鼠伤寒沙门氏菌辅助菌株反式触发肌动蛋白重排，则通过T1停靠或通过Fim粘附的非侵入性细菌可以有效入侵HeLa细胞。我们的数据表明，与HeLa细胞的结合是由至少两种不同的机制介导的，如果触发肌动蛋白重排，两者都可能导致侵袭。

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