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Reactive oxygen species (ROS) are small oxygen-derived molecules that are used to control infections by phagocytic cells. In macrophages, the oxidative burst produced by the NOX2 NADPH-oxidase is essential to eradicate engulfed pathogens by both oxidative and non-oxidative killing. Indeed, while the superoxide anion (    O  2  -    ) produced by NOX2, and the other ROS derived from its transformation, can directly target pathogens, ROS also contribute to activation of non-oxidative microbicidal effectors. The response of pathogens to the phagocytic oxidative burst includes the expression of different enzymes that target ROS to reduce their toxicity. Superoxide dismutases (SODs) are the primary scavengers ofO  2  -    , which is transformed into H 2 O 2 . In the Gram-negative  Salmonella typhimurium , periplasmic SODCI has a major role in bacterial resistance to NOX-mediated oxidative stress. In  Pseudomonas aeruginosa , the two periplasmic SODs, SODB, and SODM, appear to contribute to bacterial virulence in small-animal models. Furthermore, NOX2 oxidative stress is essential to restrict  P. aeruginosa  survival in macrophages early after infection. Here, we focused on the role of  P. aeruginosa  SODs in the counteracting of the lethal effects of the macrophage oxidative burst. Through this study of the survival of  sod  mutants in macrophages and the measurement of ROS in infected macrophages, we have identified a dual, antagonistic, role for SODB in  P. aeruginosa  survival. Indeed, the survival of the  sodB  mutants, but not of the  sodM  mutants, was greater than that of the wild-type (WT) bacteria early after infection, and  sodB -infected macrophages showed higher levels ofO  2  -and lower levels of H 2 O 2 . This suggests that SODB contributes to the production of lethal doses of H 2 O 2  within the phagosome. However, later on following infection, the  sodB  mutants survived less that the WT bacteria, which highlights the pro-survival role of SODB. We have explained this defensive role through an investigation of the activation of autophagy, which was greater in the  sodB -infected macrophages.

Escaping the Phagocytic Oxidative Burst: The Role of SODB in the Survival of Pseudomonas aeruginosa Within Macrophages