Abstract
Persisters are phenotypic variants of regular cells that exist in a dormant state with low metabolic activity, allowing them to exhibit high tolerance to antibiotics. Despite increasing recognition of their role in chronic and recalcitrant infections, the mechanisms that induce persister formation are not fully understood. In this study, we find that salicylate can induce persister formation in Escherichia coli via generation of reactive oxygen species (ROS). Salicylate-induced ROS cause a decrease in the membrane potential, reduce metabolism and lead to an increase in persistence. These effects can be recovered by culturing cells in the presence of a ROS quencher or in an anaerobic environment. Our findings reveal that salicylate-induced oxidative stress can lead to persistence, suggesting that ROS, and their subsequent impact on membrane potential and metabolism, may play a broad role in persister formation.
Highlights
Persisters are highly tolerant cells that can survive lethal doses of antibiotics by entering a dormant state[1]
We first used the fluoroquinolone ciprofloxacin, which acts by inhibiting DNA replication[19] and is effective in all cell growth phases, making it a classical antibiotic for persister isolation[20]
Salicylate has a known role in induction of antibiotic resistance through MarA9,23, the effect is modest and far below the concentrations of antibiotics we used in this study
Summary
Persisters are highly tolerant cells that can survive lethal doses of antibiotics by entering a dormant state[1]. A few recent studies have suggested that ROS can provide a protective effect against lethal doses of antibiotics by inducing bacterial persistence. Our findings suggest a pathway by which salicylate induces persistence by increasing ROS, decreasing the membrane potential and metabolism.
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