The production of endogenous hydrogen sulfide (H 2 S) has been shown to confer antibiotic tolerance in all bacteria studied to date. Therefore, this mediator has been speculated to be a universal defense mechanism against antibiotics in bacteria. This is assuming that all bacteria produce endogenous H 2 S. In this study, we established that the pathogenic bacteria Acinetobacter baumannii does not produce endogenous H 2 S, giving us the opportunity to test the effect of exogenous H 2 S on antibiotic tolerance in a bacterium that does not produce it. By using a H 2 S-releasing compound to modulate the sulfide content in A. baumannii, we demonstrated that instead of conferring antibiotic tolerance, exogenous H 2 S sensitized A. baumannii to multiple antibiotic classes, and was able to revert acquired resistance to gentamicin. Exogenous H 2 S triggered a perturbation of redox and energy homeostasis that translated into hypersensitivity to antibiotic killing. We propose that H 2 S could be used as an antibiotic-potentiator and resistance-reversion agent in bacteria that do not produce it.
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