Evidence map›Paper›PMID 29241040›Full record

ArticleCell host & microbe2017

A Large Polysaccharide Produced by Helicobacter hepaticus Induces an Anti-inflammatory Gene Signature in Macrophages.

Camille Danne, Grigory Ryzhakov, Maria Martínez-López, Nicholas Edward Ilott, Fanny Franchini, Fiona Cuskin, Elisabeth C Lowe, Samuel J Bullers, J Simon C Arthur, Fiona Powrie

Open access · hybridAbstract read
In one paragraph

Article in Cell host & microbe, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.

  1. Pooled it
  2. Cardiolipin preserves TNature metabolism · 2026
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  9. Microbiology spectrum · 2025
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  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
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  20. Article

6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Camille DanneKennedy Institute of Rheumatology, University of Oxford, Oxford, UK. Electronic address: camille.danne@gmail.com.
Grigory RyzhakovKennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
Maria Martínez-LópezImmunobiology Laboratory, Fundación Centro Nacional de Investigaciones Cardiovasculares "Carlos III" (CNIC), Melchor Fernández Almagro 3, Madrid, Spain.
Nicholas Edward IlottKennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
Fanny FranchiniKennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
Fiona CuskinInstitute for Cell and Molecular Biosciences, Medical School Newcastle University, Newcastle upon Tyne, UK.
Elisabeth C LoweInstitute for Cell and Molecular Biosciences, Medical School Newcastle University, Newcastle upon Tyne, UK.
Samuel J BullersKennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
J Simon C ArthurDivision of Cell Signaling and Immunology, School of Life Sciences, University of Dundee, Dundee, UK.
Fiona PowrieKennedy Institute of Rheumatology, University of Oxford, Oxford, UK. Electronic address: fiona.powrie@kennedy.ox.ac.uk.
University of Oxford · GBNewcastle University · GBSpanish National Centre for Cardiovascular Research · ESUniversity of Dundee · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Interactions between the host and its microbiota are of mutual benefit and promote health. Complex molecular pathways underlie this dialog, but the identity of microbe-derived molecules that mediate the mutualistic state remains elusive. Helicobacter hepaticus is a member of the mouse intestinal microbiota that is tolerated by the host. In the absence of an intact IL-10 signaling, H. hepaticus induces an IL-23-driven inflammatory response in the intestine. Here we investigate the interactions between H. hepaticus and host immune cells that may promote mutualism, and the microbe-derived molecule(s) involved. Our results show that H. hepaticus triggers early IL-10 induction in intestinal macrophages and produces a large soluble polysaccharide that activates a specific MSK/CREB-dependent anti-inflammatory and repair gene signature via the receptor TLR2. These data identify a host-bacterial interaction that promotes mutualistic mechanisms at the intestinal interface. Further understanding of this pathway may provide novel prevention and treatment strategies for inflammatory bowel disease.

Indexed as

SymbiosisAnimalsHelicobacter hepaticusImmunosuppressive AgentsInterleukin-10Interleukin-23MacrophagesMicePolysaccharides, BacterialToll-Like Receptor 2IL10 protein, mouseImmunosuppressive AgentsInterleukin-10Interleukin-23Polysaccharides, BacterialTlr2 protein, mouseToll-Like Receptor 2anti-inflammatory gene signatureCREBHelicobacter hepaticushost-microbe interactionsinflammatory bowel diseasemacrophageMSK1/2mutualismpolysaccharideTLR2

Identifiers

PMID29241040
PMCPMC5734933
OpenAlexW2773688382

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.