Evidence map›Paper›PMID 35670099›Full record

ArticleeLife2022

Fast bacterial growth reduces antibiotic accumulation and efficacy.

Urszula Łapińska, Margaritis Voliotis, Ka Kiu Lee, Adrian Campey, M Rhia L Stone, Brandon Tuck, Wanida Phetsang, Bing Zhang, Krasimira Tsaneva-Atanasova, Mark A T Blaskovich and 1 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
16.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Fast, StreamlinedChemical & biomedical imaging · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Phage provoke growth delays and SOS response induction despite CRISPR-Cas protection.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 4 countries.

Urszula ŁapińskaLiving Systems Institute, University of Exeter, Exeter, United Kingdom.ORCID 0000-0003-3593-9248
Margaritis VoliotisLiving Systems Institute, University of Exeter, Exeter, United Kingdom.ORCID 0000-0001-6488-7198
Ka Kiu LeeLiving Systems Institute, University of Exeter, Exeter, United Kingdom.
Adrian CampeyLiving Systems Institute, University of Exeter, Exeter, United Kingdom.
M Rhia L StoneCentre for Superbug Solutions, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.
Brandon TuckLiving Systems Institute, University of Exeter, Exeter, United Kingdom.
Wanida PhetsangCentre for Superbug Solutions, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.
Bing ZhangCentre for Superbug Solutions, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.
Krasimira Tsaneva-AtanasovaLiving Systems Institute, University of Exeter, Exeter, United Kingdom.ORCID 0000-0002-6294-7051
Mark A T BlaskovichCentre for Superbug Solutions, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.
Stefano PagliaraLiving Systems Institute, University of Exeter, Exeter, United Kingdom.ORCID 0000-0001-9796-1956
University of Exeter · GBThe University of Queensland · AUEngineering and Physical Sciences Research Council · GBRutgers, The State University of New Jersey · US

Funding

Medical Research Council MC_PC_17189Wellcome TrustWellcome Trust WT1104797/Z/14/Z
6 · The paper itself

Abstract

Phenotypic variations between individual microbial cells play a key role in the resistance of microbial pathogens to pharmacotherapies. Nevertheless, little is known about cell individuality in antibiotic accumulation. Here, we hypothesise that phenotypic diversification can be driven by fundamental cell-to-cell differences in drug transport rates. To test this hypothesis, we employed microfluidics-based single-cell microscopy, libraries of fluorescent antibiotic probes and mathematical modelling. This approach allowed us to rapidly identify phenotypic variants that avoid antibiotic accumulation within populations of

Indexed as

Anti-Bacterial AgentsEscherichia coli ProteinsDrug Resistance, BacterialEscherichia coliMacrolidesMicrobial Sensitivity TestsPseudomonas aeruginosaAnti-Bacterial AgentsEscherichia coli ProteinsMacrolidesantibiotic resistanceantibioticsantibiotic uptakeburkholderia cenocepaciaeffluxescherichia coliinfectious diseasemembrane transportmicrobiologymicrofluidicsphenotypic heterogeneityphysics of living systemspseudomonas aeruginosasingle-cell analysisstaphylococcus aureus

Identifiers

PMID35670099
PMCPMC9173744
OpenAlexW4281724206

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.