SodA promotes immune evasion of <i>Streptococcus suis</i> by suppressing ROS accumulation and GSDMD-mediated mitochondrial disruption in neutrophils

<i>Streptococcus suis</i> is a major swine pathogen with significant economic and zoonotic implications. Neutrophil extracellular traps (NETs) are essential for host defense, but their regulation by bacterial factors remains poorly understood. This study identifies the superoxide dismutase gene <i>sodA</i> as a key factor in immune evasion by <i>S. suis</i>. We demonstrate that <i>sodA</i> deletion enhances reactive oxygen species accumulation, mitochondrial damage, and NETs formation in neutrophils, impairing bacterial survival. These findings reveal a novel mechanism by which <i>S. suis</i> modulates host innate immunity and highlight <i>sodA</i> as a potential target for enhancing host defense against <i>S. suis</i> serotype 2 infection.