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首页> 外文期刊>Infection and immunity >Inhibition of Salmonella typhimuriumInvasion by Host Cell Expression of Secreted Bacterial Invasion Proteins
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Inhibition of Salmonella typhimuriumInvasion by Host Cell Expression of Secreted Bacterial Invasion Proteins

机译：分泌型细菌侵袭蛋白宿主细胞表达抑制鼠伤寒沙门氏菌侵袭

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Pathogenic Salmonella species initiate infection of a host by inducing their own uptake into intestinal epithelial cells. An invasive phenotype is conferred to this pathogen by a number of proteins that are components of a type III secretion system. During the invasion process, the bacteria utilize this secretion system to release proteins that enter the host cell and apparently interact with unknown host cell components that induce alterations in the actin cytoskeleton. To investigate the role of secreted proteins as direct modulators of invasion, we have evaluated the ability of Salmonella typhimurium to enter mammalian cells that express portions of theSalmonella invasion proteins SipB and SipC. Plasma membrane localization of SipB and SipC was achieved by fusing carboxyl- and amino-terminal portions of each invasion protein to the intracellular carboxyl-terminal tail of a membrane-bound eukaryotic receptor. Expression of receptor chimeras possessing the carboxyl terminus of SipB or the amino terminus of SipC blocked Salmonellainvasion, whereas expression of their chimeric counterparts had no effect on invasion. The effect on invasion was specific forSalmonella since the perturbation of uptake was not extended to other invasive bacterial species. These results suggest that Salmonella invasion can be competitively inhibited by preventing the intracellular effects of SipB or SipC. In addition, these experiments provide a model for examining interactions between bacterial invasion proteins and their host cell targets.
机译：致病性沙门氏菌物种通过诱导自身对肠道上皮细胞的吸收来引发宿主感染。这种病原体的侵入表型是由多种蛋白质构成的，这些蛋白质是III型分泌系统的组成部分。在入侵过程中，细菌利用这种分泌系统释放进入宿主细胞的蛋白质，并且显然与未知的宿主细胞组分相互作用，从而诱导肌动蛋白细胞骨架发生改变。为了研究分泌蛋白作为入侵的直接调节剂的作用，我们评估了鼠伤寒沙门氏菌进入表达沙门氏菌入侵蛋白SipB和SipC部分的哺乳动物细胞的能力。 。 SipB和SipC的质膜定位是通过将每个入侵蛋白的羧基末端和氨基末端部分融合到膜结合的真核受体的细胞内羧基末端尾部来实现的。具有SipB羧基末端或SipC氨基末端的受体嵌合体的表达阻断了沙门氏菌的侵袭，而嵌合嵌合体的表达对侵袭没有影响。沙门氏菌对入侵的影响是特异性的，因为摄取的扰动并未扩展到其他入侵细菌。这些结果表明沙门氏菌的入侵可以通过预防SipB或SipC的细胞内作用而竞争性地抑制。另外，这些实验提供了用于检查细菌入侵蛋白与其宿主细胞靶标之间相互作用的模型。

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