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首页> 外文期刊>Infection and immunity >CodY Deletion Enhances In Vivo Virulence of Community-Associated Methicillin-Resistant Staphylococcus aureus Clone USA300
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CodY Deletion Enhances In Vivo Virulence of Community-Associated Methicillin-Resistant Staphylococcus aureus Clone USA300

机译：CodY缺失增强了社区相关的耐甲氧西林金黄色葡萄球菌克隆USA300的体内毒力。

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The Staphylococcus aureus global regulator CodY responds to nutrient availability by controlling the expression of target genes. In vitro, CodY represses the transcription of virulence genes, but it is not known if CodY also represses virulence in vivo. The dominant community-associated methicillin-resistant S. aureus (CA-MRSA) clone, USA300, is hypervirulent and has increased transcription of global regulators and virulence genes; these features are reminiscent of a strain defective in CodY. Sequence analysis revealed, however, that the codY genes of USA300 and other sequenced S. aureus isolates are not significantly different from the codY genes in strains known to have active CodY. codY was expressed in USA300, as well as in other pulsotypes assessed. Deletion of codY from a USA300 clinical isolate resulted in modestly increased expression of the global regulators agr and saeRS, as well as the gene encoding the toxin alpha-hemolysin (hla). A substantial increase (>30-fold) in expression of the lukF-PV gene, encoding part of the Panton-Valentine leukocidin (PVL), was observed in the codY mutant. All of these expression differences were reversed by complementation with a functional codY gene. Moreover, purified CodY protein bound upstream of the lukSF-PV operon, indicating that CodY directly represses expression of lukSF-PV. Deletion of codY increased the virulence of USA300 in necrotizing pneumonia and skin infection. Interestingly, deletion of lukSF-PV from the codY mutant did not attenuate virulence, indicating that the hypervirulence of the codY mutant was not explained by overexpression of PVL. These results demonstrate that CodY is active in USA300 and that CodY-mediated repression restrains the virulence of USA300.
机译：金黄色葡萄球菌全局调节剂CodY通过控制靶基因的表达来响应营养物的利用。 在体外，CodY抑制毒力基因的转录，但尚不知道CodY是否在体内也能抑制毒力。与社区有关的占主导地位的耐甲氧西林金黄色葡萄球菌（CA-MRSA）克隆USA300具有高毒力，并且增加了全球调节因子和毒力基因的转录;这些特征使人联想到CodY中有缺陷的菌株。然而，序列分析表明，USA300和其他测序的金黄色葡萄球菌分离株的 codY 基因与已知具有活性CodY的菌株的 codY 基因没有显着差异。 codY 在USA300和其他评估的脉冲型中表达。从USA300临床分离株中删除 codY 导致整体调节剂 agr 和 saeRS 以及编码毒素的基因的表达适度增加α-溶血素（ hla ）。在 codY 突变体中观察到 lukF-PV 基因的表达显着增加（> 30倍），该基因编码潘顿-华伦天白蛋白（PVL）的一部分。所有这些表达差异均通过与功能性 codY 基因互补而逆转。此外，纯化的CodY蛋白与 lukSF-PV 操纵子的上游结合，表明CodY直接抑制 lukSF-PV 的表达。删除 codY 会增加USA300在坏死性肺炎和皮肤感染中的毒力。有趣的是，从 codY 突变体中删除 lukSF-PV 不会减弱毒力，这表明 codY 突变体的高毒力不能通过过表达来解释。 PVL。这些结果表明，CodY在USA300中具有活性，并且CodY介导的抑制作用抑制了USA300的毒力。

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