Evidence map›Paper›PMID 37322488›Full record

ArticleGut pathogens2023

The beneficial effects of commensal E. coli for colon epithelial cell recovery are related with Formyl peptide receptor 2 (Fpr2) in epithelial cells.

Keqiang Chen, John McCulloch, Rodrigo Das Neves, Gisele Rodrigues, Wang-Ting Hsieh, Wanghua Gong, Teizo Yoshimura, Jiaqiang Huang, Colm O'hUigin, Simone Difilippantonio and 5 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Gut pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Effects of Tumor-associatedArchives of Razi Institute · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 6 institutions in 3 countries.

Keqiang ChenLaboratory of Cancer Innovation, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702, USA. chenkeq@mail.nih.gov.
John McCullochLaboratory of Integrative Cancer Immunology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892, USA.
Rodrigo Das NevesLaboratory of Integrative Cancer Immunology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892, USA.
Gisele RodriguesLaboratory of Cancer Innovation, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702, USA.
Wang-Ting HsiehAnimal Health Diagnostic Laboratory, Frederick National Laboratory for Cancer Research, Frederick, MD, 21702, USA.
Wanghua GongBasic Research Program, Leidos Biomedical Research, Inc, Frederick, MD, 21702, USA.
Teizo YoshimuraDepartment of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8558, Japan.
Jiaqiang HuangLaboratory of Cancer Innovation, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702, USA.
Colm O'hUiginLaboratory of Integrative Cancer Immunology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892, USA.
Simone DifilippantonioGnotobiotics Facility, Frederick National Laboratory for Cancer Research, Frederick, MD, 21702, USA.
Matthew McCollumGnotobiotics Facility, Frederick National Laboratory for Cancer Research, Frederick, MD, 21702, USA.
Georgette JonesGnotobiotics Facility, Frederick National Laboratory for Cancer Research, Frederick, MD, 21702, USA.
Scott K DurumLaboratory of Cancer Innovation, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702, USA.
Giorgio TrinchieriLaboratory of Integrative Cancer Immunology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892, USA.
Ji Ming WangLaboratory of Cancer Innovation, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702, USA.
Frederick National Laboratory for Cancer Research · USNational Cancer Institute · USCenter for Cancer Research · USBeijing Jiaotong University · CNLeidos Biomedical Research Inc. (United States)Okayama University · JP

Funding

LICI Microbiome and Genetics CoreZICBC011237 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI OHUIGIN, COLM · 2009 to 2025
$28.3M
Role of mouse microbiome in cancer and inflammationZIABC011153 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TRINCHIERI, GIORGIO · 2009 to 2025
$22.0M
Role of inflammation, innate resistance, and immunity in carcinogenesis.ZIABC010793 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TRINCHIERI, GIORGIO · 2009 to 2025
$16.8M
Chronic Inflammation and CarcinogenesisZIABC011150 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DURUM, SCOTT · 2009 to 2025
$8.5M
6 · The paper itself

Abstract

backgroundFormyl peptide receptor 2 (Fpr2) plays a crucial role in colon homeostasis and microbiota balance. Commensal E. coli is known to promote the regeneration of damaged colon epithelial cells. The aim of the study was to investigate the connection between E. coli and Fpr2 in the recovery of colon epithelial cells.

resultsThe deficiency of Fpr2 was associated with impaired integrity of the colon mucosa and an imbalance of microbiota, characterized by the enrichment of Proteobacteria in the colon. Two serotypes of E. coli, O22:H8 and O91:H21, were identified in the mouse colon through complete genome sequencing. E. coli O22:H8 was found to be prevalent in the gut of mice and exhibited lower virulence compared to O91:H21. Germ-free (GF) mice that were pre-orally inoculated with E. coli O22:H8 showed reduced susceptibility to chemically induced colitis, increased proliferation of epithelial cells, and improved mouse survival. Following infection with E. coli O22:H8, the expression of Fpr2 in colon epithelial cells was upregulated, and the products derived from E. coli O22:H8 induced migration and proliferation of colon epithelial cells through Fpr2. Fpr2 deficiency increased susceptibility to chemically induced colitis, delayed the repair of damaged colon epithelial cells, and heightened inflammatory responses. Additionally, the population of E. coli was observed to increase in the colons of Fpr2

conclusionCommensal E. coli O22:H8 stimulated the upregulation of Fpr2 expression in colon epithelial cells, and the products from E. coli induced migration and proliferation of colon epithelial cells through Fpr2. Fpr2 deficiency led to an increased E. coli population in the colon and delayed recovery of damaged colon epithelial cells in mice with colitis. Therefore, Fpr2 is essential for the effects of commensal E. coli on colon epithelial cell recovery.

Indexed as

ColitisCommensal E. coliFpr2 −/− miceGerm-free miceRegeneration

Identifiers

PMID37322488
PMCPMC10268441
OpenAlexW4380841955

What OpenQuestion holds

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LicenceCC BY
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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.