Evidence map›Paper›PMID 42418657›Full record

ArticleJournal of Crohn's & colitis2026

Dietary emulsifiers and host inflammation synergistically drive genomic evolution of Crohn's disease-associated Escherichia coli toward enhanced pathogenicity.

Héloïse Rytter, Caroline Chevarin, Lucas Martin, Emma Bruder, Jérémy Denizot, Olivier Tenaillon, Olivier Espéli, Aurélien Birer, Nicolas Barnich, Emilie Viennois and 1 more

Abstract read
In one paragraph

Article in Journal of Crohn's & colitis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Héloïse RytterMicrobiome-Host Interactions, Institut Pasteur, Université Paris Cité, INSERM U1306, CNRS UMR6047, Paris, 75015, France.
Caroline ChevarinUniversité Clermont Auvergne/Inserm/U1071, USC-INRAE1382, M2iSH, Clermont-Ferrand, 63000, France.
Lucas MartinUniversité Clermont Auvergne/Inserm/U1071, USC-INRAE1382, M2iSH, Clermont-Ferrand, 63000, France.
Emma BruderCIRB-Collège de France, CNRS, INSERM, Université PSL, Paris, 75231, France.
Jérémy DenizotUniversité Clermont Auvergne/Inserm/U1071, USC-INRAE1382, M2iSH, Clermont-Ferrand, 63000, France.
Olivier TenaillonUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, 75014, France.
Olivier EspéliCIRB-Collège de France, CNRS, INSERM, Université PSL, Paris, 75231, France.
Aurélien BirerDepartment of Bacteriology, University Hospital of Clermont-Ferrand, Clermont-Ferrand, 63000, France.
Nicolas BarnichUniversité Clermont Auvergne/Inserm/U1071, USC-INRAE1382, M2iSH, Clermont-Ferrand, 63000, France.
Emilie ViennoisCenter for Research on Inflammation, UMR 1149, INSERM, Université Paris Cité, Paris, 75018, France.ORCID 0000-0002-3104-620X
Benoit ChassaingMicrobiome-Host Interactions, Institut Pasteur, Université Paris Cité, INSERM U1306, CNRS UMR6047, Paris, 75015, France.

Funding

AFA Crohn RCH FranceANR grants EMULBIONT ANR-21-CE15-0042-01DREAM ANR-20-PAMR-0002European Research Council (ERC)European Union's Horizon 2020Fondation pour la Recherche Medicale FoodHabits ENV202409018912France 2030 investment plan managed by the National Research Agency (ANR) ANR-23-IAHU-0012France 2030 investment plan managed by the National Research Agency (ANR) ANR-24-PESA-0008INSERMRégion Ile-de-France DIM BioConvergence for Health (BioConvS) and DIM One HEALTH 2.0Starting Grant ERC-2018-StG-804135Starting Grant ERC-2024-CoG-101170920the Fondation de l'Avenir AP-RM-21-032
6 · The paper itself

Abstract

BACKGROUND AND

aimsThe rising incidence of Crohn's disease (CD) in Westernized countries has been linked to changes in diet and increased consumption of food additives, yet the mechanisms by which these factors fuel intestinal inflammation remain unclear. Adherent-invasive Escherichia coli (AIEC), a pathobiont involved in CD pathogenesis, lacks a clear genetic hallmark but exhibits intestinal colonization and virulence traits, raising questions about the evolutionary forces promoting its emergence among select individuals. Here, we investigated how chronic exposure to two common dietary emulsifiers, carboxymethylcellulose (CMC) and polysorbate 80 (P80), along with host inflammation, drives AIEC genomic evolution and pathogenic potential.

methodsWild-type and Il10-deficient mice were monocolonized with AIEC and chronically exposed to CMC, P80, or water. Bacterial isolates were collected and analyzed for genomic diversification, mutations, and phenotype both in vitro and in vivo.

resultsEmulsifiers accelerated AIEC genomic diversification and selected for mutations linked to increased motility, invasion, and pro-inflammatory activity. Moreover, dietary emulsifier-evolved strains displayed a marked fitness advantage in vivo, outcompeting their counterparts in murine hosts, with the greatest advantage observed when evolution occurred under inflammatory conditions. Notably, evolutionary pathways and phenotypic outcomes were shaped by both emulsifier and the host's inflammatory status, highlighting synergy between diet and host genetics in fostering pro-inflammatory pathobionts.

conclusionThese findings provide an evolutionary framework connecting modern dietary habits to the emergence of pathogenic AIEC strains, and underscore the importance of dietary interventions in individuals at risk for inflammatory bowel disease.

Indexed as

Carboxymethylcellulose SodiumCrohn DiseaseEmulsifying AgentsEscherichia coliEscherichia coli InfectionsEvolution, MolecularPolysorbatesAnimalsInflammationMiceVirulenceCarboxymethylcellulose SodiumEmulsifying AgentsPolysorbatesAIECCrohn’s diseasedietary emulsifiergenomic evolutionpathobiont

Identifiers

PMID42418657
PMCPMC13344430

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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.