Evidence map›Paper›PMID 26698117›Full record

ArticlePloS one2015

Polymorphisms in the Toll-Like Receptor and the IL-23/IL-17 Pathways Were Associated with Susceptibility to Inflammatory Bowel Disease in a Danish Cohort.

Steffen Bank, Paal Skytt Andersen, Johan Burisch, Natalia Pedersen, Stine Roug, Julied Galsgaard, Stine Ydegaard Turino, Jacob Broder Brodersen, Shaista Rashid, Britt Kaiser Rasmussen and 7 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
6.2field-weighted citation impact, top 3% 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, 2 syntheses or guidelines pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Mucosal Responses to Type II Interferon in IBD.Inflammatory bowel diseases · 2025
    Article
  6. Article
  7. Genetic Polymorphisms ofArchives of Razi Institute · 2023
    Article
  8. Review
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  10. Review
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  12. Article
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  14. Article
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  17. Article
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  19. Article
  20. Decursin and decursinol angelate: molecular mechanism and therapeutic potential in inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Review
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

17 authors at 13 institutions in 1 country.

Steffen BankMedical Department, Viborg Regional Hospital, Viborg, Denmark.
Paal Skytt AndersenMicrobiology and Infection Control, Statens Serum Institut, Copenhagen, Denmark.
Johan BurischDepartment of Gastroenterology, Herlev Hospital, Herlev, Denmark.
Natalia PedersenDepartment of Gastroenterology, Herlev Hospital, Herlev, Denmark.
Stine RougDepartment of Gastroenterology, Hvidovre Hospital, Hvidovre, Denmark.
Julied GalsgaardMedical Department, Køge Hospital, Køge, Denmark.
Stine Ydegaard TurinoMedical Department, Hillerød Hospital, Hillerød, Denmark.
Jacob Broder BrodersenMedical Department, Sydvestjysk Hospital, Esbjerg, Denmark.
Shaista RashidMedical Department, Bispebjerg Hospital, Bispebjerg, Denmark.
Britt Kaiser RasmussenMedical Department, Nykøbing Falster Hospital, Nykøbing Falster, Denmark.
Sara AvlundMedical Department V, Aarhus University Hospital, Aarhus, Denmark.
Thomas Bastholm OlesenMedical Department, Slagelse Hospital, Slagelse, Denmark.
Hans Jürgen HoffmannDepartment of Respiratory Diseases B, Institute for Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark.
Bjørn Andersen NexøBiomedicine, University of Aarhus, Aarhus, Denmark.
Jacob SodeInstitute of Regional Health Research, University of Southern Denmark, Odense, Denmark.
Ulla VogelNational Research Centre for the Working Environment, Copenhagen, Denmark.
Vibeke AndersenMedical Department, Viborg Regional Hospital, Viborg, Denmark.
Aarhus University Hospital · DKHerlev Hospital · DKStatens Serum Institut · DKAarhus University · DKBispebjerg Hospital · DKHospital South West Jutland · DKHvidovre Hospital · DKNational Research Centre for the Working Environment · DKOdense University Hospital · DKRegionshospitalet Viborg · DKSjællands Universitetshospital, Nykøbing F. · DKSlagelse Hospital · DKZealand University Hospital Køge · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe inflammatory bowel diseases (IBD), Crohn's disease (CD) and ulcerative colitis (UC), result from the combined effects of susceptibility genes and environmental factors. Previous studies have shown that polymorphisms in the Toll-like receptor (TLR), the apoptosis, the IL-23/IL-17 and the interferon gamma (IFNG) pathways are associated with risk of both CD and UC.

methodsUsing a candidate gene approach, 21 functional single nucleotide polymorphisms (SNPs) in 15 genes were assessed in a clinical homogeneous group of severely diseased ethnic Danish patients consisting of 624 patients with CD, 411 patients with UC and 795 controls. The results were analysed using logistic regression.

resultsThe polymorphisms TLR5 (rs5744174) and IL12B (rs6887695) were associated with risk of CD, and TLR1 (rs4833095) and IL18 (rs187238) were associated with risk of both CD and UC (p<0.05). After Bonferroni correction for multiple testing, the homozygous variant genotype of TLR1 743 T>C (rs4833095) was associated with increased risk CD (OR: 3.15, 95% CI: 1.59-6.26, p = 0.02) and CD and UC combined (OR: 2.96, 95% CI: 1.64-5.32, p = 0.005).

conclusionOur results suggest that genetically determined high activity of TLR1 and TLR5 was associated with increased risk of both CD and UC and CD, respectively. This supports that the host microbial composition or environmental factors in the gut are involved in risk of IBD. Furthermore, genetically determined high activity of the IL-23/IL-17 pathway was associated with increased risk of CD and UC. Overall, our results support that genetically determined high inflammatory response was associated with increased risk of both CD and UC.

Indexed as

Genetic Predisposition to DiseaseCohort StudiesColitis, UlcerativeCrohn DiseaseFemaleGenetic Association StudiesHumansInflammatory Bowel DiseasesInterleukin-17Interleukin-23Linkage DisequilibriumLogistic ModelsMaleMetabolic Networks and PathwaysPolymorphism, Single NucleotideToll-Like ReceptorsIL17A protein, humanInterleukin-17Interleukin-23Toll-Like Receptors

Identifiers

PMID26698117
PMCPMC4689491
OpenAlexW2233843360

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.