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Staphylococcus aureus has to cope with oxidative stress during infections. In this study, S. aureus was found to be resistant to 100 mM H 2 O 2 during aerobic growth. While KatA was essential for this high aerobic H 2 O 2 resistance, the peroxiredoxin AhpC contributed to detoxification of 0.4 mM H 2 O 2 in the absence of KatA. In addition, the peroxiredoxins AhpC, Tpx and Bcp were found to be required for detoxification of cumene hydroperoxide (CHP). The high H 2 O 2 tolerance of aerobic S. aureus cells was associated with priming by endogenous H 2 O 2 levels, which was supported by an oxidative shift of the bacillithiol redox potential to -291 mV compared to -310 mV in microaerophilic cells. In contrast, S. aureus could be primed by sub-lethal doses of 100 µM H 2 O 2 during microaerophilic growth to acquire an improved resistance towards the otherwise lethal triggering stimulus of 10 mM H 2 O 2 . This microaerophilic priming was dependent on increased KatA activity, whereas aerobic cells showed constitutive high KatA activity. Thus, KatA contributes to the high H 2 O 2 resistance of aerobic cells and to microaerophilic H 2 O 2 priming in order to survive the subsequent lethal triggering doses of H 2 O 2 , allowing the adaptation of S. aureus under infections to different oxygen environments.

The Catalase KatA Contributes to Microaerophilic H2O2 Priming to Acquire an Improved Oxidative Stress Resistance in Staphylococcus aureus