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Staphylococcus aureus  is a successful human pathogen that has developed several approaches to evade the immune system, including resistance strategies to prevent oxidative killing by immune cells. One mechanism by which this evasion occurs is by production of superoxide dismutase enzymes, which require manganese as a cofactor. Manganese is acquired by the manganese transporter MntABC. One component of this operon, MntC, has been proposed as a potential vaccine candidate due to its early  in vivo  expression and its ability to provide protection in preclinical models of staphylococcal infection. In the current study, we interrogate the role of this protein in protecting  S. aureus  from oxidative stress. We demonstrate that mutation of  mntC  in a number of invasive  S. aureus  clinical isolates results in increased sensitivity to oxidative stress. In addition, we show that while downregulation of  mntC  transcription is triggered upon exposure to physiological concentrations of manganese, MntC protein is still present on the bacterial surface at these same concentrations. Taken together, these results provide insight into the role of this antigen for the pathogen.

Regulation of Staphylococcus aureus MntC Expression and Its Role in Response to Oxidative Stress