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