Evidence map›Paper›PMID 23281400›Full record

ArticleThe Journal of clinical investigation2013

NOD2-mediated dysbiosis predisposes mice to transmissible colitis and colorectal cancer.

Aurélie Couturier-Maillard, Thomas Secher, Ateequr Rehman, Sylvain Normand, Adèle De Arcangelis, Robert Haesler, Ludovic Huot, Teddy Grandjean, Aude Bressenot, Anne Delanoye-Crespin and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 340 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
340citing papers in PubMed, 3 pooled it
28.1field-weighted citation impact, top 1% 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

340 citing papers in PubMed, 3 syntheses or guidelines pooled it, 574 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Emergence of invasiveGut microbes · 2026
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  20. Resolving the field: a role for Nod2 in T cells.Journal of immunology (Baltimore, Md. : 1950) · 2025
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 6 institutions in 5 countries.

Aurélie Couturier-MaillardUniversity Lille Nord de France, Lille, France.
Thomas Secher
Ateequr Rehman
Sylvain Normand
Adèle De Arcangelis
Robert Haesler
Ludovic Huot
Teddy Grandjean
Aude Bressenot
Anne Delanoye-Crespin
Olivier Gaillot
Stefan Schreiber
Yves Lemoine
Bernhard Ryffel
David Hot
Gabriel Nùñez
Grace Chen
Philip Rosenstiel
Mathias Chamaillard
Inserm · FRCentre National de la Recherche Scientifique · FRUniversity Hospital Schleswig-Holstein · DEUniversity of Michigan · USNutrition-Génétique et Exposition aux Risques EnvironnementauxUniversity of Fribourg · CH

Funding

Nod2: A Susceptibility Gene for Crohn's DiseaseR01DK061707 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NUNEZ, GABRIEL · 2002 to 2017
$4.7M
NIDDK NIH HHS R01 DK061707
6 · The paper itself

Abstract

Instability in the composition of gut bacterial communities (dysbiosis) has been linked to common human intestinal disorders, such as Crohn's disease and colorectal cancer. Here, we show that dysbiosis caused by Nod2 deficiency gives rise to a reversible, communicable risk of colitis and colitis-associated carcinogenesis in mice. Loss of either Nod2 or RIP2 resulted in a proinflammatory microenvironment that enhanced epithelial dysplasia following chemically induced injury. The condition could be improved by treatment with antibiotics or an anti-interleukin-6 receptor-neutralizing antibody. Genotype-dependent disease risk was communicable via maternally transmitted microbiota in both Nod2-deficient and WT hosts. Furthermore, reciprocal microbiota transplantation reduced disease risk in Nod2-deficient mice and led to long-term changes in intestinal microbial communities. Conversely, disease risk was enhanced in WT hosts that were recolonized with dysbiotic fecal microbiota from Nod2-deficient mice. Thus, we demonstrated that licensing of dysbiotic microbiota is a critical component of disease risk. Our results demonstrate that NOD2 has an unexpected role in shaping a protective assembly of gut bacterial communities and suggest that manipulation of dysbiosis is a potential therapeutic approach in the treatment of human intestinal disorders.

Indexed as

AnimalsColitisColorectal NeoplasmsDigestive SystemDisease Models, AnimalFemaleHumansMaleMetagenomeMiceMice, KnockoutNod2 Signaling Adaptor ProteinPregnancyReceptor-Interacting Protein Serine-Threonine Kinase 2Receptor-Interacting Protein Serine-Threonine KinasesRisk FactorsNod2 protein, mouseNod2 Signaling Adaptor ProteinReceptor-Interacting Protein Serine-Threonine Kinase 2Receptor-Interacting Protein Serine-Threonine KinasesRipk2 protein, mouse

Identifiers

PMID23281400
PMCPMC3561825
OpenAlexW1996148181

What OpenQuestion holds

Textmetadata
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.