SodA contributes to the virulence of avian pathogenic Escherichia coli O2 strain E058 in experimentally infected chickens.

Avian pathogenic Escherichia coli (APEC), the common pathogen of avian colibacillosis, encounter reactive oxygen species (ROS) during the infection process. Superoxide dismutases (SODs), acting as antioxidant factors, can protect against ROS-mediated host defenses. Our previous reports showed that the sodA gene (encoding a Mn-cofactor-containing SOD [MnSOD]) is highly expressed during the septicemic infection process of APEC. sodA has been proved to be a virulence factor of certain pathogens, but its role in the pathogenicity of APEC has not been fully identified. In this study, we deleted the sodA gene from a virulent APEC O2 strain E058 and examined the in vitro and in vivo phenotypes of the mutant. The sodA mutant was more sensitive to hydrogen peroxide in terms of both its growth and viability. The ability to form a biofilm was weakened in the sodA mutant. The sodA mutant was significantly more easily phagocytosed than the wild-type strain by chicken macrophages. Chicken infection assays revealed significantly attenuated virulence of the sodA mutant compared with the wild-type at 24 h post-infection. The virulence phenotype was restored by complementation of the sodA gene. Quantitative real-time reverse transcription PCR revealed that the inactivation of sodA reduced the expression of oxidative stress response genes katE , perR and osmC , but did not affect the expression of sodB and sodC. Taken together, our studies indicate that SodA is important for oxidative resistance and virulence of APEC E058. IMPORTANCE Avian colibacillosis, caused by the avian pathogenic Escherichia coli , is a major bacterial disease of severe economic significance to the poultry industry worldwide. The virulence mechanisms of APEC are not completely understood. This study investigated the influence of an antioxidant protein SodA on the phenotype and pathogenicity of APEC O2 strain E058. This is the first report demonstrating that SodA plays an important role in protecting a specific APEC strain against hydrogen peroxide-induced oxidative stress and contributes to the virulence of this pathotype strain. Identification of this virulence factor will enhance our knowledge of APEC pathogenic mechanisms, which is crucial for designing successful strategies against associated infections and transmission.