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Reactivating intracellular bacterial persisters to boost antibiotic effectiveness

Nature Microbiology volume 10, pages 2661–2662 (2025)Cite this article

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A high-throughput screen that measures bacterial metabolism and host cell viability identified a host-directed compound (KL1) that reactivates intracellular bacteria that have developed antibiotic tolerance (persisters) by boosting their metabolism, which makes them susceptible to antibiotics again. KL1 enhances treatment efficacy across multiple pathogens without harming host cells.

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Fig. 1: High-throughput screen identifies compounds that sensitize intracellular bacterial persisters and improve treatment outcomes.

References

  1. Balaban, N. Q. et al. Definitions and guidelines for research on antibiotic persistence. Nat. Rev. Microbiol. 17, 441–448 (2019). This article defines antibiotic resistance, tolerance and persistence.

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  2. Helaine, S. et al. Host stress drives tolerance and persistence: the bane of anti-microbial therapeutics. Cell Host Microbe 32, 852–862 (2024). A review article on host stress and intracellular persister formation.

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  3. Rowe, S. E. et al. Reactive oxygen species induce antibiotic tolerance during systemic Staphylococcus aureus infection. Nat. Microbiol. 5, 282–290 (2020). This paper reports that host-derived ROS reduce bacterial respiration and ATP levels and increase antibiotic tolerance.

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This is a summary of: Lu, K.-Y. et al. A host-directed adjuvant sensitizes intracellular bacterial persisters to antibiotics. Nat. Microbiol. https://doi.org/10.1038/s41564-025-02124-2 (2025).

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Reactivating intracellular bacterial persisters to boost antibiotic effectiveness. Nat Microbiol 10, 2661–2662 (2025). https://doi.org/10.1038/s41564-025-02136-y

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