has to cope with oxidative stress during infections. In this study, was found to be resistant to 100 mM HO during aerobic growth. While KatA was essential for this high aerobic HO resistance, the peroxiredoxin AhpC contributed to detoxification of 0.4 mM HO 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 HO tolerance of aerobic cells was associated with priming by endogenous HO 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, could be primed by sub-lethal doses of 100 µM HO during microaerophilic growth to acquire an improved resistance towards the otherwise lethal triggering stimulus of 10 mM HO. This microaerophilic priming was dependent on increased KatA activity, whereas aerobic cells showed constitutive high KatA activity. Thus, KatA contributes to the high HO resistance of aerobic cells and to microaerophilic HO priming in order to survive the subsequent lethal triggering doses of HO, allowing the adaptation of under infections to different oxygen environments.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9495333PMC
http://dx.doi.org/10.3390/antiox11091793DOI Listing

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