Unveiling the role of sodAin Streptococcus suisserotype 2: a key regulator to neutrophil defense and NETs formation

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