Evidence map›Paper›PMID 30849075›Full record

ArticlePLoS genetics2019

Genetic effects on the commensal microbiota in inflammatory bowel disease patients.

Hugues Aschard, Vincent Laville, Eric Tchetgen Tchetgen, Dan Knights, Floris Imhann, Philippe Seksik, Noah Zaitlen, Mark S Silverberg, Jacques Cosnes, Rinse K Weersma and 4 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.6field-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

36 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
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  6. Host-pathobiont interactions in Crohn's disease.Nature reviews. Gastroenterology & hepatology · 2025
    Review
  7. Review
  8. Review
  9. Review
  10. Neutrophils: from IBD to the gut microbiota.Nature reviews. Gastroenterology & hepatology · 2024
    Review
  11. Commensal fungi in intestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2023
    Review
  12. Article
  13. Review
  14. Review
  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

14 authors at 10 institutions in 4 countries.

Hugues AschardCentre de Bioinformatique, Biostatistique et Biologie Intégrative (C3BI), Institut Pasteur, Paris, France.ORCID 0000-0002-7554-6783
Vincent LavilleCentre de Bioinformatique, Biostatistique et Biologie Intégrative (C3BI), Institut Pasteur, Paris, France.
Eric Tchetgen TchetgenDepartment of Statistics, The Wharton School at the University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Dan KnightsDepartment of Computer Science and Engineering, University of Minnesota, Minneapolis, Minnesota, United States of America.
Floris ImhannDepartment of Gastroenterology and Hepatology, University of Groningen and University Medical Center Groningen, Groningen, the Netherlands.
Philippe SeksikDepartment of Gastroenterology, Saint Antoine Hospital, Paris, France.
Noah ZaitlenDepartment of Medicine, University of California, San Francisco, California, United States of America.
Mark S SilverbergZane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, Toronto, Ontario, Canada.
Jacques CosnesDepartment of Gastroenterology, Saint Antoine Hospital, Paris, France.
Rinse K WeersmaDepartment of Gastroenterology and Hepatology, University of Groningen and University Medical Center Groningen, Groningen, the Netherlands.
Ramnik XavierBroad Institute of Harvard and MIT, Cambridge, Massachusetts, United States of America.
Laurent BeaugerieDepartment of Gastroenterology, Saint Antoine Hospital, Paris, France.
David SkurnikDivision of Infectious Diseases, Harvard Medical School, Boston, Massachusetts, United States of America.ORCID 0000-0002-4205-9639
Harry SokolDepartment of Gastroenterology, Saint Antoine Hospital, Paris, France.ORCID 0000-0002-2914-1822
Sorbonne Université · FRBroad Institute · USUniversity Medical Center Groningen · NLDélégation Paris 5 · FRHarvard University · USInserm · FRInstitut Pasteur · FRMount Sinai Hospital · CAUniversity of California, San Francisco · USUniversity of Pennsylvania · US

Funding

Impact of Genetic Variability on Cellular Pathways and Host-Microbiome InteractioU01DK062423 · NIDDK · SINAI HEALTH SYSTEM · PI MARK S. SILVERBERG · 2002 to 2026
$7.5M
Methods for Genome-wide Association Studies in Admixed PopulationsR01HG006399 · NHGRI · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI PRICE, ALKES L · 2011 to 2024
$6.3M
Identification and Inference for Longitudinal Causal Mediation Analysis in HIVR01AI104459 · NIAID · HARVARD SCHOOL OF PUBLIC HEALTH · PI SHPITSER, ILYA, VANDERWEELE, TYLER · 2013 to 2017
$2.0M
Richer Models of Asthma Risk: Bridging the Environment-Genetics DivideK25HL121295 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ZAITLEN, NOAH A · 2014 to 2018
$784k
NHGRI NIH HHS R01 HG006399NHLBI NIH HHS K25 HL121295NIAID NIH HHS R01 AI104459NIDDK NIH HHS U01 DK062423
6 · The paper itself

Abstract

Several bacteria in the gut microbiota have been shown to be associated with inflammatory bowel disease (IBD), and dozens of IBD genetic variants have been identified in genome-wide association studies. However, the role of the microbiota in the etiology of IBD in terms of host genetic susceptibility remains unclear. Here, we studied the association between four major genetic variants associated with an increased risk of IBD and bacterial taxa in up to 633 IBD cases. We performed systematic screening for associations, identifying and replicating associations between NOD2 variants and two taxa: the Roseburia genus and the Faecalibacterium prausnitzii species. By exploring the overall association patterns between genes and bacteria, we found that IBD risk alleles were significantly enriched for associations concordant with bacteria-IBD associations. To understand the significance of this pattern in terms of the study design and known effects from the literature, we used counterfactual principles to assess the fitness of a few parsimonious gene-bacteria-IBD causal models. Our analyses showed evidence that the disease risk of these genetic variants were likely to be partially mediated by the microbiome. We confirmed these results in extensive simulation studies and sensitivity analyses using the association between NOD2 and F. prausnitzii as a case study.

Indexed as

AdultCARD Signaling Adaptor ProteinsEubacterialesFaecalibacterium prausnitziiFemaleGastrointestinal MicrobiomeGenetic Association StudiesGenetic Predisposition to DiseaseGenetic VariationHost Microbial InteractionsHumansInflammatory Bowel DiseasesMaleMiddle AgedModels, GeneticNod2 Signaling Adaptor ProteinCARD9 protein, humanCARD Signaling Adaptor ProteinsNOD2 protein, humanNod2 Signaling Adaptor Protein

Identifiers

PMID30849075
PMCPMC6426259
OpenAlexW2922059288

What OpenQuestion holds

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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.