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Abstract
Bacterial persister cells are phenotypic variants that exhibit a transient non-growing state and antibiotic tolerance. Here, we provide in vitro evidence of Staphylococcus aureus persisters within infected host cells. We show that the bacteria surviving antibiotic treatment within host cells are persisters, displaying biphasic killing and reaching a uniformly non-responsive, non-dividing state when followed at the single-cell level. This phenotype is stable but reversible upon antibiotic removal. Intracellular S. aureus persisters remain metabolically active but display an altered transcriptomic profile consistent with activation of stress responses, including the stringent response as well as cell wall stress, SOS and heat shock responses. These changes are associated with multidrug tolerance after exposure to a single antibiotic. We hypothesize that intracellular S. aureus persisters may constitute a reservoir for relapsing infection and could contribute to therapeutic failures.
Highlights
Bacterial persister cells are phenotypic variants that exhibit a transient non-growing state and antibiotic tolerance
Persisters are usually evidenced by biphasic kill curves, when a bulk of susceptible bacteria is rapidly killed by exposure to high antibiotic concentrations, while a small proportion survives for longer time[2,3]
Intracellular survival of Staphylococcus aureus is widely recognized as a major factor in the recurrence of infections[16] and intracellular forms of S. aureus have been shown to become less responsive to antibiotic action[17], suggesting a switch to a persister phenotype
Summary
Bacterial persister cells are phenotypic variants that exhibit a transient non-growing state and antibiotic tolerance. We show that the bacteria surviving antibiotic treatment within host cells are persisters, displaying biphasic killing and reaching a uniformly non-responsive, non-dividing state when followed at the single-cell level. This phenotype is stable but reversible upon antibiotic removal. Intracellular S. aureus persisters remain metabolically active but display an altered transcriptomic profile consistent with activation of stress responses, including the stringent response as well as cell wall stress, SOS and heat shock responses. These changes are associated with multidrug tolerance after exposure to a single antibiotic. Intracellular survival of Staphylococcus aureus is widely recognized as a major factor in the recurrence of infections[16] and intracellular forms of S. aureus have been shown to become less responsive to antibiotic action[17], suggesting a switch to a persister phenotype
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