Elucidating the contributions of superoxide dismutases to staphylococcus aureus pathogenicity

Bacterial infections are a leading cause of death worldwide. One disease-causing organism is Staphylococcus aureus. Despite numerous methods used by the host immune system to combat infection, S. aureus is still a major health risk. Recently, the Centers for Disease Control and Prevention and the World Health Organization listed S. aureus as one of the top threats to human health [15, 88]. The elevated threat is due to an increase of antibiotic resistant isolates and continued prevalence in the general community [15, 88], which calls for the development of new therapeutic targets to treat staphylococcal infections. In order to combat S. aureus infections, their disease causing mechanisms need to be better understood. One of the many virulence factors of S. aureus to cause disease are superoxide dismutases (SODs). In S. aureus there are two superoxide dismutases, SodA and SodM. The loss of both SODs during a retro-orbital mouse infection led to a decrease in the ability of S. aureus to cause disease [65]. However, the individual contributions of SodA and SodM to the pathogenesis of S. aureus are not completely understood. In this work I aimed to identify how SodA and SodM provide protection to S. aureus and contribute to combating nutritional immunity