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首页> 外文期刊>Infection and immunity >Yersinia pseudotuberculosis-Induced Calcium Signaling in Neutrophils Is Blocked by the Virulence Effector YopH
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Yersinia pseudotuberculosis-Induced Calcium Signaling in Neutrophils Is Blocked by the Virulence Effector YopH

机译：致病性因子YopH阻断中性粒细胞中耶尔森氏菌假结核诱导的钙信号传导。

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Pathogenic species of the genus Yersinia evade the bactericidal functions of phagocytes. This evasion is mediated through their virulence effectors, Yops, which act within target cells. In this study we investigated the effect of Yersinia pseudotuberculosis on Ca2+ signaling in polymorphonuclear neutrophils. The intracellular free calcium concentration in single adherent human neutrophils was monitored during bacterial infection and, in parallel, the encounter between the bacteria and cells was observed. When a plasmid-cured strain was used for infection, adherence of a single bacterium to the cellular surface induced a β1 integrin-dependent transient increase in the intracellular concentration of free calcium. This was, however, not seen with Yop-expressing wild-type bacteria, which adhered to the cell surface without generating any Ca2+ signal. Importantly, the overall Ca2+homeostasis was not affected by the wild-type strain; the Ca2+ signal mediated by the G-protein-coupled formyl-methionyl-leucyl-phenylalanine receptor was still functioning. Hence, the blocking effect was restricted to certain receptors and their signaling pathways. The use of different Yop mutant strains revealed that the protein tyrosine phosphatase YopH was responsible for the inhibition. This virulence determinant has previously been implicated in very rapid Yersinia-mediated effects on target cells as the key effector in the blockage of phagocytic uptake. The present finding, that Y. pseudotuberculosis, via YopH, specifically inhibits a self-induced immediate-early Ca2+ signal in neutrophils, offers more-detailed information concerning the effectiveness of this virulence effector and implies an effect on Ca2+-dependent, downstream signals.
机译：耶尔森氏菌属的致病菌种具有吞噬细胞的杀菌功能。这种逃避是通过它们在靶细胞内起作用的毒力效应因子Yops介导的。在这项研究中，我们研究了假性耶尔森氏菌对多形核中性粒细胞Ca 2 + 信号的影响。在细菌感染过程中监测单个粘附的人类嗜中性粒细胞的细胞内游离钙浓度，并同时观察到细菌与细胞之间的相遇。当使用质粒固化的菌株进行感染时，单一细菌粘附到细胞表面会诱导β 1 整合素依赖性细胞内游离钙浓度的瞬时增加。然而，表达Yop的野生型细菌没有看到这种现象，它附着在细胞表面而没有产生任何Ca 2 + 信号。重要的是，整个Ca 2 + 体内稳态不受野生型菌株的影响。 G蛋白偶联的甲酰基-甲硫酰基-亮氨酰-苯丙氨酸受体介导的Ca 2 + 信号仍在起作用。因此，阻断作用仅限于某些受体及其信号传导途径。使用不同的Yop突变株表明，酪氨酸磷酸酶YopH引起了抑制。以前，这种毒力决定因素与耶尔森菌介导的对靶细胞的快速作用有关，是吞噬细胞阻断作用的关键效应物。目前的发现是 Y。假结核病通过YopH特异地抑制嗜中性粒细胞中自我诱导的立即早期Ca 2 + 信号，提供了有关该毒力效应物有效性的更多详细信息，并暗示了对Ca的影响 2 + 相关的下游信号。

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