Evidence map›Paper›PMID 33027280›Full record

ArticlePLoS pathogens2020

Lipopolysaccharide O structure of adherent and invasive Escherichia coli regulates intestinal inflammation via complement C3.

Masashi Ohno, Mizuho Hasegawa, Atsushi Hayashi, Gustavo Caballero-Flores, Christopher J Alteri, Trevor D Lawley, Nobuhiko Kamada, Gabriel Núñez, Naohiro Inohara

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Microbiology (Reading, England) · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Potential role of microbiota in ovarian cancer treatment.Archives of medical science : AMS · 2025
    Article
  7. Role of adherent invasiveWorld journal of clinical cases · 2022
    Review
  8. Review
  9. DietaryFrontiers in veterinary science · 2022
    Article
  10. Article
  11. Article
  12. Two EnteropathogenicJournal of microbiology and biotechnology · 2021
    Article
  13. Article
  14. Diversity and Adaptations ofMicroorganisms · 2021
    Article
  15. Oral pathobiontGut microbes
    Article
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

9 authors at 4 institutions in 3 countries.

Masashi OhnoDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.ORCID 0000-0003-3505-7835
Mizuho HasegawaDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.ORCID 0000-0002-4108-2773
Atsushi HayashiInternal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.ORCID 0000-0003-4060-2383
Gustavo Caballero-FloresRogel Cancer Center, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.
Christopher J AlteriDepartment of Natural Sciences, University of Michigan-Dearborn, Dearborn, Michigan, United States of America.ORCID 0000-0002-6367-5684
Trevor D LawleyWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, United Kingdom.
Nobuhiko KamadaInternal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.ORCID 0000-0002-1980-4178
Gabriel NúñezDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.ORCID 0000-0002-6529-2695
Naohiro InoharaDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.ORCID 0000-0002-4215-9349
University of Michigan · USMichigan United · USShiga University of Medical Science · JPWellcome Sanger Institute · GB

Funding

University of Michigan Center for Gastrointestinal ResearchP30DK034933 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI OWYANG, CHUNG · 1986 to 2021
$22.5M
Reciprocal Control of Motility and Adherence in UTIR01AI059722 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PEARSON, MELANIE M. · 2005 to 2024
$7.4M
The role of IL-1ß-inducing pathobionts in the pathogenesis of Crohn’s diseaseR01DK108901 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Nobuhiko Kamada · 2017 to 2026
$3.8M
Role of Immunity and the Microbiota in Enteropathogenic E. coli EradicationR01DK095782 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NUNEZ, GABRIEL · 2013 to 2022
$3.6M
The Role of Inflammasomes in Mucosal Immunity to Intestinal Bacterial PathogensR01DK091191 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NUNEZ, GABRIEL · 2010 to 2019
$3.1M
The link between oral bacteria and gut diseaseR01DK119219 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAMADA, NOBUHIKO · 2019 to 2022
$1.6M
Periodontitis and extra-oral mucosal inflammationR21AI142047 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAMADA, NOBUHIKO · 2019 to 2020
$429k
NIAID NIH HHS R01 AI059722NIAID NIH HHS R21 AI142047NIDDK NIH HHS P30 DK034933NIDDK NIH HHS R01 DK091191NIDDK NIH HHS R01 DK095782NIDDK NIH HHS R01 DK108901NIDDK NIH HHS R01 DK119219
6 · The paper itself

Abstract

Gut dysbiosis associated with intestinal inflammation is characterized by the blooming of particular bacteria such as adherent-invasive E. coli (AIEC). However, the precise mechanisms by which AIEC impact on colitis remain largely unknown. Here we show that antibiotic-induced dysbiosis worsened chemically-induced colitis in IL-22-deficient mice, but not in wild-type mice. The increase in intestinal inflammation was associated with the expansion of E. coli strains with genetic and functional features of AIEC. These E. coli isolates exhibited high ability to out compete related bacteria via colicins and resistance to the host complement system in vitro. Mutation of wzy, the lipopolysaccharide O polymerase gene, rendered AIEC more sensitive to the complement system and more susceptible to engulfment and killing by phagocytes while retaining its ability to outcompete related bacteria in vitro. The wzy AIEC mutant showed impaired fitness to colonize the intestine under colitic conditions, but protected mice from chemically-induced colitis. Importantly, the ability of the wzy mutant to protect from colitis was blocked by depletion of complement C3 which was associated with impaired intestinal eradication of AIEC in colitic mice. These studies link surface lipopolysaccharide O-antigen structure to the regulation of colitic activity in commensal AIEC via interactions with the complement system.

Indexed as

AnimalsBacterial AdhesionComplement C3Crohn DiseaseEscherichia coliEscherichia coli InfectionsInflammationIntestinal MucosaLipopolysaccharidesMice, Inbred C57BLComplement C3Lipopolysaccharides

Identifiers

PMID33027280
PMCPMC7571687
OpenAlexW3092362091

What OpenQuestion 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 OpenQuestion graph.