ArticleNature communications2017
Time-programmable drug dosing allows the manipulation, suppression and reversal of antibiotic drug resistance in vitro.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed.
- Contezolid and polymyxin B nonapeptide combination reveals antibacterial synergy against multidrug-resistant Acinetobacter baumannii strains.BMC microbiology · 2026Article
- Evolutionary drivers of divergent collateral sensitivity responses during antibiotic therapy.Nature ecology & evolution · 2026Review
- Unlocking the potential of experimental evolution to study drug resistance in pathogenic fungi.npj antimicrobials and resistance · 2024Review
- Collateral sensitivity counteracts the evolution of antifungal drug resistance in Candida auris.Nature microbiology · 2024Article
- Article
- Distinguishing mutants that resist drugs via different mechanisms by examining fitness tradeoffs.eLife · 2024Article
- In Vitro Resistance-Predicting Studies and In Vitro Resistance-Related Parameters-A Hit-to-Lead Perspective.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Distinguishing mutants that resist drugs via different mechanisms by examining fitness tradeoffs.bioRxiv : the preprint server for biology · 2024Article
- Laboratory Evolution of Antimicrobial Resistance in Bacteria to Develop Rational Treatment Strategies.Antibiotics (Basel, Switzerland) · 2024Review
- Sequential antibiotic therapy in the laboratory and in the patient.Journal of the Royal Society, Interface · 2023Article
- Antibiotics Limit Adaptation of Drug-Resistant Staphylococcus aureus to Hypoxia.Antimicrobial agents and chemotherapy · 2022Article
- Article
- Investigations into the antibacterial effects and potential mechanism of gambogic acid and neogambogic acid.Frontiers in microbiology · 2022Article
- Leveraging laboratory and clinical studies to design effective antibiotic combination therapy.Current opinion in microbiology · 2021Review
- Identification of antibiotic pairs that evade concurrent resistance via a retrospective analysis of antimicrobial susceptibility test results.The Lancet. Microbe · 2021Article
- Design principles of collateral sensitivity-based dosing strategies.Nature communications · 2021Article
- Drug-induced resistance evolution necessitates less aggressive treatment.PLoS computational biology · 2021Article
- Article
- Article
- Fighting microbial pathogens by integrating host ecosystem interactions and evolution.BioEssays : news and reviews in molecular, cellular and developmental biology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Multi-drug strategies have been attempted to prolong the efficacy of existing antibiotics, but with limited success. Here we show that the evolution of multi-drug-resistant Escherichia coli can be manipulated in vitro by administering pairs of antibiotics and switching between them in ON/OFF manner. Using a multiplexed cell culture system, we find that switching between certain combinations of antibiotics completely suppresses the development of resistance to one of the antibiotics. Using this data, we develop a simple deterministic model, which allows us to predict the fate of multi-drug evolution in this system. Furthermore, we are able to reverse established drug resistance based on the model prediction by modulating antibiotic selection stresses. Our results support the idea that the development of antibiotic resistance may be potentially controlled via continuous switching of drugs.
Indexed as
Identifiers
What OpenQuestion holds
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.