Evidence map›Paper›PMID 26161647›Full record

ArticlePloS one2015

Toll-Like Receptor 4 Wild Type Homozygozity of Polymorphisms +896 and +1196 Is Associated with High Gastrin Serum Levels and Peptic Ulcer Risk.

Vesa-Matti Pohjanen, Olli-Pekka Koivurova, Heikki Huhta, Olli Helminen, Johanna M Mäkinen, Jari M Karhukorpi, Tapio Joensuu, Pentti O Koistinen, Jarno M Valtonen, Seppo E Niemelä and 2 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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.7field-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

4 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Association of Toll-like receptor 4 single-nucleotide polymorphisms Asp299Gly and Thr399Ile with the risk of primary open angle glaucoma.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2017
    Article
  3. The Expression of Toll-like Receptors in Normal Human and Murine Gastrointestinal Organs and the Effect of Microbiome and Cancer.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2016
    Article
  4. Article
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

12 authors at 3 institutions in 1 country.

Vesa-Matti PohjanenMedical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland.
Olli-Pekka KoivurovaDepartment of Internal Medicine, Oulu University Hospital, Oulu, Finland.
Heikki HuhtaMedical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland.
Olli HelminenMedical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland.
Johanna M MäkinenMedical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland.
Jari M KarhukorpiDepartment of Medical Microbiology and Immunology, Institute of Diagnostics, University of Oulu, Oulu, Finland; Eastern Finland Laboratory Centre Joint Authority Enterprise (ISLAB), Joensuu, Finland.
Tapio JoensuuMedical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland; Department of Internal Medicine, Pietarsaari City Hospital, Pietarsaari, Finland.
Pentti O KoistinenOulu City Hospital, Oulu, Finland.
Jarno M ValtonenOulu City Hospital, Oulu, Finland.
Seppo E NiemeläDepartment of Internal Medicine, Oulu University Hospital, Oulu, Finland.
Riitta A KarttunenDepartment of Medical Microbiology and Immunology, Institute of Diagnostics, University of Oulu, Oulu, Finland.
Tuomo J KarttunenMedical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland.
Oulu University Hospital · FIUniversity of Oulu · FIEastern Finland Laboratory Center · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptor 4 is a part of the innate immune system and recognizes Helicobacter pylori lipopolysaccharide. The goal of this study was to analyze the role of Toll-like receptor 4 polymorphisms +896 (rs4986790) and +1196 (rs4986791) in the pathogenesis of Helicobacter pylori related gastroduodenal diseases in relation to gastric secretion and inflammation. Toll-like receptor 4 polymorphisms, serum gastrin-17 and pepsinogen I and II concentrations were determined, and gastroscopies with histopathological analyses were performed to 216 dyspeptic patients. As genotype controls, 179 controls and 61 gastric cancer patients were studied. In our study, the Toll-like receptor 4 +896 and +1196 polymorphisms were in total linkage disequilibrium. The homozygous wild types displayed higher gastrin-17 serum concentrations than the mutants (p = 0.001) and this effect was independent of Helicobacter pylori. The homozygous wild types also displayed an increased risk for peptic ulcers (OR: 4.390). Toll-like receptor 4 genotypes did not show any association with Helicobacter pylori positivity or the features of gastric inflammation. Toll-like receptor 4 expression was seen in gastrin and somatostatin expressing cells of antral mucosa by immunohistochemistry. Our results suggest a role for Toll-like receptor 4 in gastric acid regulation and that the Toll-like receptor 4 +896 and +1196 wild type homozygozity increases peptic ulcer risk via gastrin secretion.

Indexed as

Polymorphism, Single NucleotideAdultAgedAged, 80 and overFemaleGastrinsGastritisGene FrequencyGenetic Predisposition to DiseaseGenotypeHelicobacter InfectionsHelicobacter pyloriHumansImmunohistochemistryMaleMiddle Agedgastrin 17GastrinsPepsinogen APepsinogen CTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID26161647
PMCPMC4498789
OpenAlexW1541516662

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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.