Data：Unveiling the role of sodA in Streptococcus suis serotype 2: a key regulator to neutrophil defense and NETs formation

Streptococcus suis serotype 2 (SS2) is a major porcine pathogen. Neutrophil extracellular traps (NETs) can capture and kill pathogens, which is an essential mechanism of action of neutrophils against pathogens. However, the key genes and mechanisms of SS2-induced NETs formation remain unclear. Our study explored the role of sodA in SS2-induced neutrophil infection, with a particular focus on NETs. We found that the intraperitoneally injected sodA deletion (ΔsodA) SS2 strain recruited fewer neutrophils than the wild-type (WT) SS2 strain. Neutrophils were isolated and infected with WT or ΔsodA. The results showed that deletion of sodA reduced the bactericidal effect of SS2 on neutrophils by reducing the induction of NETs. Moreover, compared with WT, ΔsodA caused a more significant disruption of the mitochondrial membrane potential and increased reactive oxygen species levels. As GSDMD is a pore-forming protein, we investigated the role of GSDMD-N in the mitochondrial membranes during SS2 infection. The results showed that GSDMD-N contracts with mitochondria. In conclusion, sodA deficiency attenuates the ability to induce NETs in SS2 and appears to disrupt the mitochondrial membrane through the expression of GSDMD-N.

猪链球菌2型（Streptococcus suis serotype 2，SS2）是一种主要的猪源致病菌。中性粒细胞胞外陷阱（Neutrophil extracellular traps，NETs）能够捕获并杀灭病原体，是中性粒细胞对抗病原体的核心作用机制。然而，SS2诱导NETs形成的关键基因及分子机制仍不明确。本研究探讨了sodA在SS2诱导的中性粒细胞感染过程中的作用，重点聚焦于NETs的形成。研究发现，腹腔注射sodA缺失（ΔsodA）SS2菌株后，其招募的中性粒细胞数量较野生型（WT）SS2菌株更少。我们分离中性粒细胞并分别用WT或ΔsodA菌株进行感染，结果显示，sodA的缺失通过削弱SS2对NETs的诱导能力，降低了SS2对中性粒细胞的杀菌效应。此外，与WT菌株相比，ΔsodA菌株可更显著地破坏线粒体膜电位，并升高活性氧水平。鉴于焦孔素D（GSDMD）是一种成孔蛋白，我们进一步探究了GSDMD-N端结构域（GSDMD-N）在SS2感染过程中在线粒体膜上的作用。结果显示，GSDMD-N可与线粒体发生结合。综上，sodA缺失可减弱SS2诱导中性粒细胞形成NETs的能力，且该过程似乎通过GSDMD-N的表达破坏线粒体膜来实现。