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Bacterial persisters—dormant cells with a high tolerance for antibiotic treatment—are prime culprits in chronic and recurrent infections. James J. Collins and coworkers at Boston University show that indole-based bacterial communication plays a key role in increasing bacterial persistence (Nat. Chem. Biol., DOI: 10.1038/nchembio.915). They incubated cultures of Escherichia coli with physiological levels of indole for one hour and then treated the cultures with high levels of three antibiotics. The bacteria showed distinct levels of persistence in response to various antibiotics, but indole increased persistence in each case by at least an order of magnitude. Engineered bacteria unable to generate indole from the amino acid tryptophan formed fewer persisters, but bacteria with impaired indole uptake likewise formed fewer persisters, which suggests that indole-induced persistence was in response to indole concentrations outside rather than inside the cells. Collins and coworkers found that indole triggers protective pathways such as the phage shock and oxidative stress responses. The researchers call such communication a “bet-hedging strategy” that the bacteria can adjust in response to environmental cues.
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