Evidence map›Paper›PMID 29965986›Full record

ArticlePloS one2018

The presence of genetic risk variants within PTPN2 and PTPN22 is associated with intestinal microbiota alterations in Swiss IBD cohort patients.

Bahtiyar Yilmaz, Marianne R Spalinger, Luc Biedermann, Yannick Franc, Nicolas Fournier, Jean-Benoit Rossel, Pascal Juillerat, Gerhard Rogler, Andrew J Macpherson, Michael Scharl

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 50 citations in OpenAlex.

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  12. The Gut Microbiota in Inflammatory Bowel Disease.Frontiers in cellular and infection microbiology · 2022
    Review
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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

10 authors at 3 institutions in 1 country.

Bahtiyar YilmazMaurice Müller Laboratories, Department for Biomedical Research, University of Bern, Bern, Switzerland.ORCID 0000-0003-1888-9226
Marianne R SpalingerDepartment of Gastroenterology and Hepatology, University Hospital Zürich, University of Zürich, Zürich, Switzerland.
Luc BiedermannDepartment of Gastroenterology and Hepatology, University Hospital Zürich, University of Zürich, Zürich, Switzerland.
Yannick FrancInstitute of Social and Preventive Medicine (IUMSP), Lausanne University Hospital, Lausanne, Switzerland.
Nicolas FournierInstitute of Social and Preventive Medicine (IUMSP), Lausanne University Hospital, Lausanne, Switzerland.
Jean-Benoit RosselInstitute of Social and Preventive Medicine (IUMSP), Lausanne University Hospital, Lausanne, Switzerland.
Pascal JuilleratMaurice Müller Laboratories, Department for Biomedical Research, University of Bern, Bern, Switzerland.ORCID 0000-0002-0947-5235
Gerhard RoglerDepartment of Gastroenterology and Hepatology, University Hospital Zürich, University of Zürich, Zürich, Switzerland.
Andrew J MacphersonMaurice Müller Laboratories, Department for Biomedical Research, University of Bern, Bern, Switzerland.
Michael ScharlDepartment of Gastroenterology and Hepatology, University Hospital Zürich, University of Zürich, Zürich, Switzerland.ORCID 0000-0002-6729-1469
University of Zurich · CHInstitute of Social and Preventive Medicine · CHUniversity of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenetic risk factors, intestinal microbiota and a dysregulated immune system contribute to the pathogenesis of inflammatory bowel disease (IBD). We have previously demonstrated that dysfunction of protein tyrosine phosphatase non-receptor type 2 (PTPN2) and PTPN22 contributes to alterations of intestinal microbiota and the onset of chronic intestinal inflammation in vivo. Here, we investigated the influence of PTPN2 and PTPN22 gene variants on intestinal microbiota composition in IBD patients.

methodsBacterial DNA from mucosa-associated samples of 75 CD and 57 UC patients were sequenced using 16S rRNA sequencing approach. Microbial analysis, including alpha diversity, beta diversity and taxonomical analysis by comparing to PTPN2 (rs1893217) and PTPN22 (rs2476601) genotypes was performed in QIIME, the phyloseq R package and MaAsLin pipeline.

resultsIn PTPN2 variant UC patients, we detected an increase in relative abundance of unassigned genera from Clostridiales and Lachnospiraceae families and reduction of Roseburia when compared to PTPN2 wild-type (WT) patients. Ruminoccocus was increased in PTPN22 variant UC patients. In CD patients with severe disease course, Faecalibacterium, Bilophila, Coprococcus, unclassified Erysipelotrichaeceae, unassigned genera from Clostridiales and Ruminococcaceae families were reduced and Bacteroides were increased in PTPN2 WT carriers, while Faecalibacterium, Bilophila, Coprococcus, and Erysipelotrichaeceae were reduced in PTPN22 WT patients when compared to patients with mild disease. In UC patients with severe disease, relative abundance of Lachnobacterium was reduced in PTPN2 and PTPN22 WT patients, Dorea was increased in samples from PTPN22 WT carriers and an unassigned genus from Ruminococcaceae gen. was increased in patients with PTPN2 variant genotype.

conclusionsWe identified that IBD-associated genetic risk variants, disease severity and the interaction of these factors are related to significant alterations in intestinal microbiota composition of IBD patients.

Indexed as

Disease SusceptibilityGastrointestinal MicrobiomeGenetic VariationAdultAllelesBiopsyCohort StudiesFemaleGenetic Predisposition to DiseaseGenotypeHumansInflammatory Bowel DiseasesMaleMiddle AgedModels, BiologicalPolymorphism, Single NucleotideProtein Tyrosine Phosphatase, Non-Receptor Type 2Protein Tyrosine Phosphatase, Non-Receptor Type 22PTPN22 protein, humanPTPN2 protein, humanRNA, Ribosomal, 16S

Identifiers

PMID29965986
PMCPMC6028086
OpenAlexW2811384188

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.