Evidence map›Paper›PMID 40640200›Full record

ArticleNature communications2025

Vancomycin-resistant enterococci utilise antibiotic-enriched nutrients for intestinal colonisation.

Olivia G King, Alexander Y G Yip, Victoria Horrocks, Jesús Miguéns Blanco, Julian R Marchesi, Benjamin H Mullish, Thomas B Clarke, Julie A K McDonald

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

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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

8 authors.

Olivia G KingDepartment of Life Sciences, Centre for Bacterial Resistance Biology, Imperial College London, London, UK.
Alexander Y G YipDepartment of Life Sciences, Centre for Bacterial Resistance Biology, Imperial College London, London, UK.ORCID http://orcid.org/0000-0003-3681-122X
Victoria HorrocksDepartment of Life Sciences, Centre for Bacterial Resistance Biology, Imperial College London, London, UK.ORCID http://orcid.org/0000-0003-4662-4321
Jesús Miguéns BlancoDivision of Digestive Diseases, Department of Metabolism, Digestion and Reproduction, Faculty of Medicine, St Mary's Hospital Campus, Imperial College London, London, UK.ORCID http://orcid.org/0000-0001-7725-965X
Julian R MarchesiDivision of Digestive Diseases, Department of Metabolism, Digestion and Reproduction, Faculty of Medicine, St Mary's Hospital Campus, Imperial College London, London, UK.ORCID http://orcid.org/0000-0002-7994-5239
Benjamin H MullishDivision of Digestive Diseases, Department of Metabolism, Digestion and Reproduction, Faculty of Medicine, St Mary's Hospital Campus, Imperial College London, London, UK.ORCID http://orcid.org/0000-0001-6300-3100
Thomas B ClarkeDepartment of Infectious Disease, Centre for Bacterial Resistance Biology, Imperial College London, London, UK.ORCID http://orcid.org/0000-0002-9997-9532
Julie A K McDonaldDepartment of Life Sciences, Centre for Bacterial Resistance Biology, Imperial College London, London, UK. julie.mcdonald@imperial.ac.uk.ORCID http://orcid.org/0000-0003-0739-6047

Funding

Imperial College London Start-up funds from the Department of Life SciencesWellcome TrustWellcome Trust (Wellcome) 227795/Z/23/Z
6 · The paper itself

Abstract

Antibiotic treatment significantly disrupts the gut microbiome and promotes vancomycin-resistant enterococci (VRE) intestinal colonisation. These disruptions cause the intestine to act as a reservoir for VRE that seed difficult-to-treat infections. Here we show that antibiotics that promote VRE intestinal colonisation increase the concentration of a wide range of nutrients and decrease the concentration of a wide range of microbial metabolites. We show significant but incomplete suppression of VRE growth by individual short chain fatty acids that were decreased in antibiotic-treated faecal microbiomes. However, mixtures of short chain fatty acids provide complete or near complete suppression of VRE growth. We show that VRE use most nutrients increased in antibiotic-treated faecal microbiomes as carbon or nitrogen sources to support their growth, where Enterococcus faecium and Enterococcus faecalis have some common and some distinct preferences for the use of these specific nutrients. Finally, we show that E. faecium and E. faecalis occupy overlapping but distinct nutrient-defined intestinal niches that promote high growth when cultured with each other and when cultured with carbapenem-resistant Enterobacteriaceae. Our results demonstrate that VRE occupy distinct intestinal niches in the antibiotic-treated intestine, defined by their abilities to utilise specific enriched nutrients and their abilities to grow with reduced concentrations of inhibitory microbial metabolites.

Indexed as

Anti-Bacterial AgentsGastrointestinal MicrobiomeIntestinesNutrientsVancomycin-Resistant EnterococciAnimalsCarbonEnterococcus faecalisEnterococcus faeciumFatty Acids, VolatileFecesGram-Positive Bacterial InfectionsHumansNitrogenAnti-Bacterial AgentsCarbonFatty Acids, VolatileNitrogenNutrients

Identifiers

PMID40640200
PMCPMC12246219

What OpenQuestion holds

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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.