Evidence map›Paper›PMID 26650186›Full record

ArticleMolecular medicine (Cambridge, Mass.)2016

GPR84 and TREM-1 Signaling Contribute to the Pathogenesis of Reflux Esophagitis.

Heba Abdel-Aziz, Mathias Schneider, Winfried Neuhuber, Abdel Meguid Kassem, Saleem Khailah, Jürgen Müller, Hadeel Gamal Eldeen, Ahmed Khairy, Mohamed T Khayyal, Anastasiia Shcherbakova and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

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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

12 authors at 4 institutions in 2 countries.

Heba Abdel-AzizDepartment of Pharmacology, Institute of Pharmaceutical Chemistry, Westfalian Wilhelms University, Münster, Germany.
Mathias SchneiderDepartment of Pharmaceutical Biology, Institute of Pharmacy and Biochemistry, Johannes Gutenberg University, Mainz, Germany.
Winfried NeuhuberInstitute of Anatomy, University of Erlangen-Nürnberg, Erlangen, Germany.
Abdel Meguid KassemTropical Medicine Department and Gastrointestinal Endoscopy Unit, Faculty of Medicine, Cairo University, Cairo, Egypt.
Saleem KhailahTropical Medicine Department and Gastrointestinal Endoscopy Unit, Faculty of Medicine, Cairo University, Cairo, Egypt.
Jürgen MüllerScientific Department, Steigerwald Arzneimittelwerk GmbH, Darmstadt, Germany.
Hadeel Gamal EldeenTropical Medicine Department and Gastrointestinal Endoscopy Unit, Faculty of Medicine, Cairo University, Cairo, Egypt.
Ahmed KhairyTropical Medicine Department and Gastrointestinal Endoscopy Unit, Faculty of Medicine, Cairo University, Cairo, Egypt.
Mohamed T KhayyalDepartment of Pharmacology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
Anastasiia ShcherbakovaMedical Clinic III, University Clinic Centre, Rheinische Friedrich-Wilhelms University, Bonn, Germany.
Thomas EfferthDepartment of Pharmaceutical Biology, Institute of Pharmacy and Biochemistry, Johannes Gutenberg University, Mainz, Germany.
Gudrun Ulrich-MerzenichMedical Clinic III, University Clinic Centre, Rheinische Friedrich-Wilhelms University, Bonn, Germany.
Cairo University · EGJohannes Gutenberg University Mainz · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastro-esophageal reflux disease (GERD) is one of the most common disorders in gastroenterology. Patients present with or without increased acid exposure indicating a nonuniform etiology. Thus, the common treatment with proton pump inhibitors (PPIs) fails to control symptoms in up to 40% of patients. To further elucidate the pathophysiology of the condition and explore new treatment targets, transcriptomics, proteomics and histological methods were applied to a surgically induced subchronic reflux esophagitis model in Wistar rats after treatment with either omeprazole (PPI) or STW5, a herbal preparation shown to ameliorate esophagitis without affecting refluxate pH. The normal human esophageal squamous cell line HET-1A and human endoscopic biopsies were used to confirm our findings to the G-protein-coupled receptor (GPR) 84 in human tissue. Both treatments reduced reflux-induced macroscopic and microscopic lesions of the esophagi as well as known proinflammatory cytokines. Proteomic and transcriptomic analyses identified CINC1-3, MIP-1/3α, MIG, RANTES and interleukin (IL)-1β as prominent mediators in GERD. Most regulated cyto-/chemokines are linked to the TREM-1 signaling pathway. The fatty acid receptor GPR84 was upregulated in esophagitis but significantly decreased in treated groups, a finding supported by Western blot and immunohistochemistry in both rat tissue and HET-1A cells. GPR84 was also found to be significantly upregulated in patients with grade B reflux esophagitis. The expression of GPR84 in esophageal tissue and its potential involvement in GERD are reported for the first time. IL-8 (CINC1-3) and the TREM-1 signaling pathway are proposed, besides GPR84, to play an important role in the pathogenesis of GERD.org.

Identifiers

PMID26650186
PMCPMC4982478
OpenAlexW2439190156

What OpenQuestion holds

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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.