Superoxide dismutase of Streptococcus suis serotype 2 plays a role in anti-autophagic response by scavenging reactive oxygen species in infected macrophages

Streptococcus suis serotype 2 (SS2) causes septic shock and meningitis. However, its pathogenesis is still not well-understood. We have recently shown that superoxide dismutase sodA of SS2 is a virulence factor probably by increasing resistance to oxidative stresses. Reactive oxygen species (ROS) are products of the respiratory burst of phagocytic cells and have been shown to activate autophagy. We wanted to know if and how SS2 explores its sodA to interfere with cell autophagic responses. A sodA deletion mutant (Δsod) was compared with its parent and complemented strain in autophagic response in the murine macrophage cell line RAW264.7. We found that the Δsod mutant induced significant autophagic responses in infected cells, shown as increased LC3 lipidation (LC3-II) and EGFP-LC3 punctae, than those infected by its parent or complemented strain at 1 or 2h post-infection. Co-localization of the autophagosomal EGFP-LC3 vesicles with lysosomes was seen in cells infected with Δsod mutant and its parent strain, indicating that SS2 infection induced complete autophagic responses. Reduced autophagic responses of cells infected with the wild-type strain might be related to decreased ROS by the scavenging effect of its sodA, as shown by increased superoxide anion or ROS level in cells infected with the Δsod mutant and in the cell free xanthine oxidase-hypoxanthine ROS-generating system, as compared with its parent or complemented strain. Taken together, SS2 makes use of its sodA for survival not only by scavenging ROS but also by alleviating the host autophagic responses due to ROS stimulation.

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