猪链球菌2型可抑制猪中性粒细胞形成胞外诱捕网（NETs），这无疑是该菌逃避NETs捕杀效应、成功建立感染并导致猪严重发病的重要机制之一。本研究拟通过Label-free比较蛋白质组学方法分析G+菌的模式分子PGN（肽聚糖）诱导猪中性粒细胞形成NETs时的差异蛋白，筛选并鉴定其激活的主要信号通路。在此基础上研究猪链球菌2型对信号通路激活NETs的抑制效应，从而鉴定猪链球菌抑制NETs形成的主要信号通路。同时基于构建的重组表达猪链球菌表面蛋白和分泌蛋白的“文库”，筛选可显著抑制猪NETs形成的关键因子。通过相应基因的缺失突变体和回复突变菌株，确认该基因在抑制猪NETs形成通路中的作用。力图阐明猪链球菌2型是通过表达哪些（个）蛋白来抑制哪条（些）信号途径，而抑制猪中性粒细胞形成NETs、从而逃避其杀菌效应的分子机制。为深入解析猪链球菌2型的免疫逃避机制奠定重要基础。

Streptococcus suis serotype 2 (SS2) could inhibit swine neutrophils to form extracellular traps (NETs), which plays an essential role in clearance of bacteria. It would benefit the bacteria to evade NETs-mediate killing, which was one of the essential reasons that the bacteria could infect pigs and cause severe diseases. The present study would analyze the differentially expressed proteins of PGN (peptidoglycan, a pattern recognized molecular of Gram-positive bacteria)-induced swine neutrophils or mock treated neutrophils by label-free quantitative proteomics. And then we would identify the major swine signaling pathways for PGN-induced NETs with the activator and blocking reagent. On the basis of these results, the present study would identify the NETs formatting related signaling pathways which can be inhibited by SS2. Meanwhile, we would also identify the bacterial evasion-related factors by screening the recombinant SS2 surface proteins and secreted proteins pool. After that, the potential bacterial evasion-related factors would be confirmed and characterized by specific gene-deletion experiments and complementary experiments. The aim of this study was to clarify the mechanism how SS2 evade PGN-induced NETs formatting and subsequent host killing. It would contribute to the pathogenesis of SS2 diseases.