Evidence map›Paper›PMID 35413017›Full record

ArticleJCI insight2022

Mucosal metabolites fuel the growth and virulence of E. coli linked to Crohn's disease.

Shiying Zhang, Xochitl Morgan, Belgin Dogan, Francois-Pierre Martin, Suzy Strickler, Akihiko Oka, Jeremy Herzog, Bo Liu, Scot E Dowd, Curtis Huttenhower and 9 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 30 citations in OpenAlex.

  1. Trial
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  4. Deciphering the Implications ofPathogens (Basel, Switzerland) · 2026
    Review
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  7. Article
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  11. Host-pathobiont interactions in Crohn's disease.Nature reviews. Gastroenterology & hepatology · 2025
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. 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

19 authors at 8 institutions in 6 countries.

Shiying ZhangDepartment of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA.
Xochitl MorganDepartment of Microbiology and Immunology, University of Otago, Dunedin, New Zealand.
Belgin DoganDepartment of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA.
Francois-Pierre MartinNestlé Institute of Health Sciences, Nestlé Research, Société des Produits Nestlé S.A., Lausanne, Switzerland.
Suzy StricklerBoyce Thompson Institute, Cornell University, Ithaca, New York, USA.
Akihiko OkaShimane University Faculty of Medicine, Shimane, Japan.
Jeremy HerzogDepartment of Medicine, Center for Gastrointestinal Biology and Disease, University of North Carolina (UNC) at Chapel Hill, North Carolina, USA.
Bo LiuDepartment of Medicine, Center for Gastrointestinal Biology and Disease, University of North Carolina (UNC) at Chapel Hill, North Carolina, USA.
Scot E DowdMolecular Research LP, Shallowater, Texas, USA.
Curtis HuttenhowerBiostatistics Department, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.
Matthieu PichaudEnterome, Paris, France.
Esra I DoganDepartment of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA.
Jack SatsangiTranslational Gastroenterology Unit, Nuffield Department of Medicine, John Radcliffe Hospital Oxford, United Kingdom.
Randy LongmanJill Roberts Center for Inflammatory Bowel Disease, Weill Cornell Medical College, Cornell University, New York, New York, USA.
Rhonda YantissJill Roberts Center for Inflammatory Bowel Disease, Weill Cornell Medical College, Cornell University, New York, New York, USA.
Lukas A MuellerBoyce Thompson Institute, Cornell University, Ithaca, New York, USA.
Ellen J ScherlJill Roberts Center for Inflammatory Bowel Disease, Weill Cornell Medical College, Cornell University, New York, New York, USA.
R Balfour SartorDepartment of Medicine, Center for Gastrointestinal Biology and Disease, University of North Carolina (UNC) at Chapel Hill, North Carolina, USA.
Kenneth W SimpsonDepartment of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA.
Cornell University · USUniversity of North Carolina at Chapel Hill · USEnterome (France) · FRHarvard University · USJohn Radcliffe Hospital · GBNestlé (Switzerland) · CHShimane University · JPUniversity of Otago · NZ

Funding

Role of IL-10 in APC Regulation of Protective vs. Pathogenic T Cell Responses toP01DK094779 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SHEIKH, SHEHZAD Z. · 2013 to 2023
$17.9M
National Gnotobiotic Rodent Resource CenterP40OD010995 · OD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Ryan B Sartor · 2012 to 2026
$9.7M
Host-Microbiota Interactions in Crohn's Disease-associated SpondyloarthritisR01DK114252 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI LONGMAN, RANDY S · 2018 to 2022
$1.9M
NIDDK NIH HHS P01 DK094779NIDDK NIH HHS R01 DK114252NIH HHS P40 OD010995
6 · The paper itself

Abstract

Elucidating how resident enteric bacteria interact with their hosts to promote health or inflammation is of central importance to diarrheal and inflammatory bowel diseases across species. Here, we integrated the microbial and chemical microenvironment of a patient's ileal mucosa with their clinical phenotype and genotype to identify factors favoring the growth and virulence of adherent and invasive E. coli (AIEC) linked to Crohn's disease. We determined that the ileal niche of AIEC was characterized by inflammation, dysbiosis, coculture of Enterococcus, and oxidative stress. We discovered that mucosal metabolites supported general growth of ileal E. coli, with a selective effect of ethanolamine on AIEC that was augmented by cometabolism of ileitis-associated amino acids and glutathione and by symbiosis-associated fucose. This metabolic plasticity was facilitated by the eut and pdu microcompartments, amino acid metabolism, γ-glutamyl-cycle, and pleiotropic stress responses. We linked metabolism to virulence and found that ethanolamine and glutamine enhanced AIEC motility, infectivity, and proinflammatory responses in vitro. We connected use of ethanolamine to intestinal inflammation and L-fuculose phosphate aldolase (fucA) to symbiosis in AIEC monoassociated IL10-/- mice. Collectively, we established that AIEC were pathoadapted to utilize mucosal metabolites associated with health and inflammation for growth and virulence, enabling the transition from symbiont to pathogen in a susceptible host.

Indexed as

Crohn DiseaseEscherichia coli InfectionsAnimalsBacterial AdhesionEscherichia coliEthanolaminesHealth PromotionInflammationIntestinal MucosaMiceVirulenceEthanolaminesAmino acid metabolismInflammationInflammatory bowel diseaseMicrobiology

Identifiers

PMID35413017
PMCPMC9220930
OpenAlexW4223418177

What Socratic 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 Socratic graph.