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Analysis on Actinobacillus pleuropneumoniae LuxS regulated genes reveals pleiotropic roles of LuxS/AI-2 on biofilm formation, adhesion ability and iron metabolism

机译:胸膜肺炎放线杆菌LuxS调控基因的分析揭示了LuxS / AI-2对生物膜形成,粘附能力和铁代谢的多效作用

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摘要

LuxS is an enzyme involved in the activated methyl cycle and the by-product autoinducer-2 (AI-2) was a quorum sensing signal in some species. In our previous study, the functional LuxS in AI-2 production was verified in the porcine respiratory pathogen Actinobacillus pleuropneumoniae. Enhanced biofilm formation and reduced virulence were observed in the luxS mutant. To comprehensively understand the luxS function, in this study, the transcriptional profiles were compared between the A. pleuropneumoniae luxS mutant and its parental strain in four different growth phases using microarray. Many genes associated with infection were differentially expressed. The biofilm formation genes pgaABC in the luxS mutant were up-regulated in early exponential phase, while 9 genes associated with adhesion were down-regulated in late exponential phase. A group of genes involved in iron acquisition and metabolism were regulated in four growth phases. Phenotypic investigations using luxS mutant and both genetic and chemical (AI-2) complementation on these virulence traits were performed. The results demonstrated that the luxS mutant showed enhanced biofilm formation and reduced adhesion ability and these effects were not due to lack of AI-2. But AI-2 could increase biofilm formation and adhesion of A. pleuropneumoniae independent of LuxS. Growth under iron restricted condition could be controlled by LuxS through AI-2 production. These results revealed pleiotropic roles of LuxS and AI-2 on A. pleuropneumoniae virulence traits
机译:LuxS是一种参与活化甲基循环的酶,副产物autoinducer-2(AI-2)在某些物种中是群体感应信号。在我们以前的研究中,在猪呼吸道病原体胸膜肺炎放线杆菌中已验证了AI-2生产中的功能性LuxS。在luxS突变体中观察到增强的生物膜形成和降低的毒力。为了全面了解luxS功能,在本研究中,使用微阵列比较了胸膜肺炎链球菌luxS突变体及其亲本菌株在四个不同生长阶段的转录谱。与感染相关的许多基因被差异表达。 luxS突变体中的生物膜形成基因pgaABC在指数早期被上调,而与粘附相关的9个基因在指数晚期被下调。一组与铁的获取和代谢有关的基因在四个生长阶段受到调控。使用luxS突变体以及这些毒力特性的遗传和化学(AI-2)互补进行表型调查。结果表明,luxS突变体显示出增强的生物膜形成和降低的粘附能力,并且这些作用不是由于缺乏AI-2而引起的。但是AI-2可以增加独立于LuxS的胸膜肺炎链球菌的生物膜形成和粘附。 LuxS可通过AI-2生产来控制铁受限条件下的生长。这些结果揭示了LuxS和AI-2对胸膜肺炎链球菌毒力特性的多效性作用。

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