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Role of the luxS Quorum-Sensing System in Biofilm Formation and Virulence of Staphylococcus epidermidis

机译:luxS群体感应系统在表皮葡萄球菌生物膜形成和致病性中的作用

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Nosocomial infections caused by Staphylococcus epidermidis are characterized by biofilm formation on implanted medical devices. Quorum-sensing regulation plays a major role in the biofilm development of many bacterial pathogens. Here, we describe luxS, a quorum-sensing system in staphylococci that has a significant impact on biofilm development and virulence. We constructed an isogenic ΔluxS mutant strain of a biofilm-forming clinical isolate of S. epidermidis and demonstrated that luxS signaling is functional in S. epidermidis. The mutant strain showed increased biofilm formation in vitro and enhanced virulence in a rat model of biofilm-associated infection. Genetic complementation and addition of autoinducer 2-containing culture filtrate restored the wild-type phenotype, demonstrating that luxS repressed biofilm formation through a cell-cell signaling mechanism based on autoinducer 2 secretion. Enhanced production of the biofilm exopolysaccharide polysaccharide intercellular adhesin in the mutant strain is presumably the major cause of the observed phenotype. The agr quorum-sensing system has previously been shown to impact biofilm development and biofilm-associated infection in a way similar to that of luxS, although by regulation of different factors. Our study indicates a general scheme of quorum-sensing regulation of biofilm development in staphylococci, which contrasts with that observed in many other bacterial pathogens.
机译:表皮葡萄球菌引起的医院感染的特征是在植入的医疗器械上形成生物膜。群体感应调节在许多细菌病原体的生物膜发育中起主要作用。在这里,我们描述了 luxS ,这是一种葡萄球菌的群体感应系统,对生物膜的发育和毒力具有重大影响。我们构建了 S的生物膜形成临床分离株的同基因ΔluxS突变株。并证明 luxS 信号在 S中起作用。表皮动物。该突变株在体外生物膜相关感染的大鼠模型中显示出增加的生物膜形成和增强的毒力。遗传互补和添加含有自诱导物2的培养物滤液恢复了野生型表型,表明 luxS 通过基于自诱导物2分泌的细胞信号机制抑制了生物膜的形成。推测突变株中生物膜胞外多糖多糖胞间粘附素的产量增加可能是观察到的表型的主要原因。以前已经证明, agr 群体感应系统以与 luxS 类似的方式影响生物膜的发育和与生物膜相关的感染,尽管通过不同因素的调节。我们的研究表明在葡萄球菌中群体感应调节生物膜发育的一般方案,这与在许多其他细菌病原体中观察到的相反。

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