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Background  The phagocytic oxidative burst is a primary effector of innate immunity that protects against bacterial infection. However, the mechanism by which reactive oxygen species (ROS) kill or inhibit bacteria is not known. It is often assumed that DNA is a primary target of oxidative damage, consistent with known effects of endogenously produced ROS in the bacterial cytoplasm. But most studies fail to distinguish between effects of host derived ROS versus damage caused by endogenous bacterial sources. We took advantage of both the ability of  Salmonella enterica  serovar Typhimurium to survive in macrophages and the genetic tractability of the system to test the hypothesis that phagocytic superoxide damages cytoplasmic targets including DNA.    Methodology/Principal Findings  SodCI is a periplasmic Cu-Zn superoxide dismutase (SOD) that contributes to the survival of  Salmonella  Typhimurium in macrophages. Through competitive virulence assays, we asked if  sodCI  has a genetic interaction with various cytoplasmic systems. We found that SodCI acts independently of cytoplasmic SODs, SodA and SodB. In addition, SodCI acts independently of the base excision repair system and RuvAB, involved in DNA repair. Although  sodCI  did show genetic interaction with  recA , this was apparently independent of recombination and is presumably due to the pleiotropic effects of a  recA  mutation.    Conclusions/Significance  Taken together, these results suggest that bacterial inhibition by phagocytic superoxide is primarily the result of damage to an extracytoplasmic target.

Phagocytic Superoxide Specifically Damages an Extracytoplasmic Target to Inhibit or Kill Salmonella