ArticlePLoS pathogens2024
Intoxication of antibiotic persisters by host RNS inactivates their efflux machinery during infection.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 9 citations in OpenAlex.
- Bacterial strategies for surviving antibiotics during urinary tract infection: could uropathogenic Escherichia coli be persisters?Nature reviews. Urology · 2026Review
- Building-block synthesis as a determinant of antibiotic persistence.Nature communications · 2026Article
- Contributions of persisters and the Eagle effect to survival ofMicrobiology spectrum · 2026Article
- Mechanism of persister formation in response to nitrogen starvation.Nature communications · 2026Article
- Review
- Article
- Molecular Basis of Persister Awakening and Lag-Phase Recovery inInternational journal of molecular sciences · 2026Review
- A host-directed adjuvant sensitizes intracellular bacterial persisters to antibiotics.Nature microbiology · 2025Article
- Disruption of sulfur transferase complex increases bacterial intramacrophage persistence.PLoS pathogens · 2025Article
- Antibiotic-recalcitrant Salmonella during infection.Nature reviews. Microbiology · 2025Review
- Host stress drives tolerance and persistence: The bane of anti-microbial therapeutics.Cell host & microbe · 2024Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The host environment is of critical importance for antibiotic efficacy. By impacting bacterial machineries, stresses encountered by pathogens during infection promote the formation of phenotypic variants that are transiently insensitive to the action of antibiotics. It is assumed that these recalcitrant bacteria-termed persisters-contribute to antibiotic treatment failure and relapsing infections. Recently, we demonstrated that host reactive nitrogen species (RNS) transiently protect persisters against the action of β-lactam antibiotics by delaying their regrowth within host cells. Here, we discovered that RNS intoxication of persisters also collaterally sensitizing them to fluoroquinolones during infection, explaining the higher efficiency of fluoroquinolones against intramacrophage Salmonella. By reducing bacterial respiration and the proton-motive force, RNS inactivate the AcrAB efflux machinery of persisters, facilitating the accumulation of fluoroquinolones intracellularly. Our work shows that target inactivity is not the sole reason for Salmonella persisters to withstand antibiotics during infection, with active efflux being a major contributor to survival. Thus, understanding how the host environment impacts persister physiology is critical to optimize antibiotics efficacy during infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.