Evidence map›Paper›PMID 28860510›Full record

Observational studyScientific reports2017

A functional IL1RL1 variant regulates corticosteroid-induced sST2 expression in ulcerative colitis.

David Díaz-Jiménez, Lucía Núñez, Marjorie De la Fuente, Karen Dubois-Camacho, Hugo Sepúlveda, Martín Montecino, Alejandro Torres-Riquelme, Paulina García-González, Jonás Chnaiderman, Anna Vossenkamper and 6 more

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
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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

16 authors at 5 institutions in 3 countries.

David Díaz-JiménezDisciplinary Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, CL, 8380453, Chile.
Lucía NúñezDisciplinary Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, CL, 8380453, Chile.
Marjorie De la FuenteDisciplinary Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, CL, 8380453, Chile.
Karen Dubois-CamachoDisciplinary Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, CL, 8380453, Chile.
Hugo SepúlvedaCenter for Biomedical Research, Faculty of Biological Sciences and Faculty of Medicine, and FONDAP Centre for Genome Regulation, Universidad Andres Bello, Santiago, Chile.
Martín MontecinoCenter for Biomedical Research, Faculty of Biological Sciences and Faculty of Medicine, and FONDAP Centre for Genome Regulation, Universidad Andres Bello, Santiago, Chile.
Alejandro Torres-RiquelmeDisciplinary Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, CL, 8380453, Chile.
Paulina García-GonzálezDisciplinary Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, CL, 8380453, Chile.
Jonás ChnaidermanDisciplinary Program of Virology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, CL, 8380453, Chile.ORCID 0000-0003-2541-523X
Anna VossenkamperCentre for Immunobiology, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Thomas T MacDonaldCentre for Immunobiology, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Daniela SimianSubdirección de Investigación, Dirección Académica, Clínica Las Condes, Santiago, CL, 7591018, Chile.
María-Julieta GonzálezCell and Molecular Biology Program, Biomedical Sciences Institute, Faculty of Medicine, Universidad de Chile, Santiago, CL, 8380453, Chile.
John A CidlowskiLaboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
Rodrigo QueraGastroenterology Unit, Clínica Las Condes, Santiago, CL, 7591018, Chile. rquera@clinicalascondes.cl.
Marcela A HermosoDisciplinary Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, CL, 8380453, Chile. mhermoso@med.uchile.cl.
University of Chile · CLClínica Las Condes · CLNational Institutes of Health · USQueen Mary University of London · GBUniversidad Andrés Bello · CL

Funding

Medical Research Council G0800746
6 · The paper itself

Abstract

The ST2/IL33 signalling pathway has been associated with ulcerative colitis (UC). ST2, encoded by the IL1RL1 gene, is expressed as both a membrane-anchored receptor (ST2L) activated by IL33 and as a soluble receptor (sST2) with anti-inflammatory properties. In UC patients, sST2 is further increased by corticosteroid treatment; however, the glucocorticoid-mediated molecular regulation remains unknown. We therefore tested whether genetic variants in the IL1RL1 distal promoter are involved in UC and affect glucocorticoid-mediated ST2 expression. Serum ST2 levels and genetic variants in the IL1RL1 distal promoter were examined by ELISA and PCR sequencing in UC patients receiving corticosteroids. Glucocorticoid-mediated ST2 production was evaluated in intestinal mucosa cultures. Molecular regulation of glucocorticoid-mediated ST2 was assessed by RT-qPCR, ChIP assay and luciferase reporter assay. Dexamethasone effect on ST2 transcript expression was analyzed in leukocytes and related to IL1RL1 variants. Sequencing of a distal IL1RL1 promoter region demonstrated that SNPs rs6543115(C) and rs6543116(A) are associated with increased sST2 in UC patients on corticosteroids. Dexamethasone up-regulated sST2 transcription through interaction with the glucocorticoid-response element (GRE) carrying rs6543115(C) variant. Our data indicate that IL1RL1 SNPs rs6543115(C) confer susceptibility to UC and is contained in the GRE, which may modulate glucocorticoid-induced sST2 expression.

Indexed as

Polymorphism, Single NucleotideUp-RegulationAdrenal Cortex HormonesAdultCells, CulturedColitis, UlcerativeDexamethasoneFemaleGene Expression RegulationGenetic Predisposition to DiseaseHumansInterleukin-1 Receptor-Like 1 ProteinIntestinal MucosaMaleMiddle AgedPromoter Regions, GeneticAdrenal Cortex HormonesDexamethasoneIL1RL1 protein, humanInterleukin-1 Receptor-Like 1 Protein

Identifiers

PMID28860510
PMCPMC5579262
OpenAlexW2746137726

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.