Evidence map›Paper›PMID 40113753›Full record

ArticleNature communications2025

Sublethal systemic LPS in mice enables gut-luminal pathogens to bloom through oxygen species-mediated microbiota inhibition.

Sanne Kroon, Dejan Malcic, Lena Weidert, Lea Bircher, Leonardo Boldt, Philipp Christen, Patrick Kiefer, Anna Sintsova, Bidong D Nguyen, Manja Barthel and 13 more

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

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  14. Systematic evaluation of metatranscriptomic differential gene expressionbioRxiv : the preprint server for biology · 2025
    Article
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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

23 authors.

Sanne KroonInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.ORCID http://orcid.org/0000-0002-5722-0763
Dejan MalcicInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.
Lena WeidertInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.
Lea BircherInstitute of Food, Nutrition and Health, Department of Health Sciences and Technology, ETH Zürich, Zürich, Switzerland.
Leonardo BoldtInterfaculty Institute of Microbiology and Infection Medicine Tübingen, University of Tübingen, Tübingen, Germany.ORCID http://orcid.org/0009-0009-7743-605X
Philipp ChristenInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.ORCID http://orcid.org/0000-0002-3139-2874
Patrick KieferInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.
Anna SintsovaInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.
Bidong D NguyenInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.
Manja BarthelInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.
Yves SteigerInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.ORCID http://orcid.org/0000-0002-8048-250X
Melanie ClercInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.ORCID http://orcid.org/0000-0003-1195-4558
Mathias K-M HerzogInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.
Carmen ChenInfectious Diseases Service, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
Ersin GülInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.
Benoit GueryInfectious Diseases Service, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
Emma SlackInstitute of Food, Nutrition and Health, Department of Health Sciences and Technology, ETH Zürich, Zürich, Switzerland.ORCID http://orcid.org/0000-0002-2473-1145
Shinichi SunagawaInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.ORCID http://orcid.org/0000-0003-3065-0314
Julia A VorholtInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.ORCID http://orcid.org/0000-0002-6011-4910
Lisa MaierInterfaculty Institute of Microbiology and Infection Medicine Tübingen, University of Tübingen, Tübingen, Germany.ORCID http://orcid.org/0000-0002-6473-4762
Christophe LacroixInstitute of Food, Nutrition and Health, Department of Health Sciences and Technology, ETH Zürich, Zürich, Switzerland.ORCID http://orcid.org/0000-0003-4360-2020
Annika HausmannInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland. annika.hausmann@hest.ethz.ch.ORCID http://orcid.org/0000-0001-8852-3444
Wolf-Dietrich HardtInstitute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland. hardt@micro.biol.ethz.ch.ORCID http://orcid.org/0000-0002-9892-6420

Funding

EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 Marie Skłodowska-Curie Actions (H2020 Excellent Science - Marie Skłodowska-Curie Actions) 956279Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation) 310030_192567Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation) 51NF40_180575
6 · The paper itself

Abstract

Endotoxin-driven systemic immune activation is a common hallmark across various clinical conditions. During acute critical illness, elevated plasma lipopolysaccharide triggers non-specific systemic immune activation. In addition, a compositional shift in the gut microbiota, including an increase in gut-luminal opportunistic pathogens, is observed. Whether a causal link exists between acute endotoxemia and abundance of gut-luminal opportunistic pathogens is incompletely understood. Here, we model acute, pathophysiological lipopolysaccharide concentrations in mice and show that systemic exposure promotes a 100-10'000-fold expansion of Klebsiella pneumoniae, Escherichia coli, Enterococcus faecium and Salmonella Typhimurium in the gut within one day, without overt enteropathy. Mechanistically, this is driven by a Toll-like receptor 4-dependent increase in gut-luminal oxygen species levels, which transiently halts microbiota fermentation and fuels growth of gut-luminal facultative anaerobic pathogens through oxidative respiration. Thus, systemic immune activation transiently perturbs microbiota homeostasis and favours opportunistic pathogens, potentially increasing the risk of infection in critically ill patients.

Indexed as

Gastrointestinal MicrobiomeLipopolysaccharidesReactive Oxygen SpeciesAnimalsEndotoxemiaEnterococcus faeciumEscherichia coliFemaleKlebsiella pneumoniaeMaleMiceMice, Inbred C57BLSalmonella typhimuriumToll-Like Receptor 4LipopolysaccharidesReactive Oxygen SpeciesTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID40113753
PMCPMC11926250

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Registered trials

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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.