Identification and proteome analysis of the two-component VirR/VirS system in epidemic Streptococcus suis serotype 2.
Identification and proteome analysis of the two-component VirR/VirS system in epidemic Streptococcus suis serotype 2.
复制标题
DOI：
10.1111/j.1574-6968.2012.02611.x
复制
发表时间：
2012-08
影响因子：
2.1
通讯作者：
Haihui Wang;Xiaodong Shen;Yan Zhao;Min Wang;Qiu Zhong;Tian Chen;F. Hu;Ming Li
中科院分区：
文献类型：
--
作者：
Haihui Wang;Xiaodong Shen;Yan Zhao;Min Wang;Qiu Zhong;Tian Chen;F. Hu;Ming Li
猪链球菌2型(SS2)是一种重要的人畜共患病病原体，可感染猪，也可引起人的严重感染。中国近日发生两起高死亡率人链球菌中毒性休克综合征大规模暴发疫情，对全球公共卫生提出了新的挑战。然而，对流行的SS2分离株毒力的全球调控缺乏系统的了解。在这项研究中，我们对与产气荚膜梭菌的VirR/VIRS调控系统同源的SS2双组分系统进行了突变和功能分析。VIRs(ΔVirs)的等位基因敲除突变体表现出明显的表型变化，包括形成更短的链和更薄的囊壁，更容易在全血中清除，并降低氧化应激耐力。此外，ΔVIRRS突变体在小鼠模型中显著减弱。对野生型毒株和ΔVIRRS突变体的表达谱进行比较蛋白质组分析，我们可以鉴定出72个在没有VIRR/VIRS系统的情况下差异表达的蛋白质，这些蛋白质直接导致ΔVIRRS突变体的多效性表型。
Streptococcus suis serotype 2 (SS2) is an important zoonotic pathogen that infects pigs and sporadically causes serious infections in humans. Two recent large-scale outbreaks of human streptococcal toxic-shock-like syndrome with high mortality occurred in China, posing new challenges for global public health. However, the global regulation of the virulence of epidemic SS2 isolates lacks a systematic understanding. In this study, we performed a mutational and functional analysis of an SS2 two-component system that is orthologous to the VirR/VirS regulatory system of Clostridium perfringens. An isogenic knockout mutant of VirR/VirS (ΔvirRS) was found to exhibit marked phenotypic changes, including the formation of shorter chains and thinner capsular walls, more easily cleared in whole blood, and decreased oxidative stress tolerance. Furthermore, the ΔvirRS mutant was greatly attenuated in a mouse model. Comparative proteome analysis of the expression profiles of the wild-type strain with the ΔvirRS mutant allowed us to identify 72 proteins that are differentially expressed in the absence of the VirR/VirS system and that are directly responsible for the pleiotropic phenotype of the ΔvirRS mutant.