Evidence map›Paper›PMID 25091434›Full record

ArticleThe Journal of allergy and clinical immunology2015

Phenotypic and genotypic association of epithelial IL1RL1 to human TH2-like asthma.

Russell S Traister, Crystal E Uvalle, Gregory A Hawkins, Deborah A Meyers, Eugene R Bleecker, Sally E Wenzel

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 62 citations in OpenAlex.

  1. Targeting IL-33 in Precision Neuroimmunology: Cellular Mechanisms and Therapeutic Strategies for CNS Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  2. Article
  3. Article
  4. The Influence of Genetic Polymorphisms ofInternational journal of dentistry · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Emerging Effects of IL-33 on COVID-19.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Interleukin-33: Its Emerging Role in Allergic Diseases.Molecules (Basel, Switzerland) · 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

6 authors at 2 institutions in 1 country.

Russell S TraisterDepartment of Medicine, University of Pittsburgh, Pittsburgh, Pa. Electronic address: traisterrs@upmc.edu.
Crystal E UvalleDepartment of Medicine, University of Pittsburgh, Pittsburgh, Pa.
Gregory A HawkinsCenter for Genomics and Personalized Medicine Research, Wake Forest School of Medicine, Winston-Salem, NC.
Deborah A MeyersCenter for Genomics and Personalized Medicine Research, Wake Forest School of Medicine, Winston-Salem, NC.
Eugene R BleeckerCenter for Genomics and Personalized Medicine Research, Wake Forest School of Medicine, Winston-Salem, NC.
Sally E WenzelDepartment of Medicine, University of Pittsburgh, Pittsburgh, Pa.
University of Pittsburgh · USWake Forest University · US

Funding

UNIVERSITY OF PITTSBURGH CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTE: BPCAUL1RR024153 · NCRR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2006 to 2011
$73.9M
University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8M
Translational Training Program in Pulmonary Biology and MedicineT32HL007563 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Melanie Koenigshoff · 1985 to 2026
$12.3M
Redox-Derived Pulmonary Anti-Inflammatory MediatorsR01HL064937 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 2000 to 2015
$5.6M
TGF-BETA AND 15 HETE IN POORLY STEROID RESPONSIVE ASTHMAR01AI040600 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WENZEL, SALLY E · 1997 to 2014
$4.8M
Implications and Stability of Clinical and Molecular Phenotypes of Severe AsthmaU10HL109152 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WENZEL, SALLY E · 2011 to 2016
$3.9M
NCATS NIH HHS UL1 TR000005NCRR NIH HHS UL1 RR024153NHLBI NIH HHS HL064937-10NHLBI NIH HHS HL-109152-01NHLBI NIH HHS HL-69437NHLBI NIH HHS R01 HL064937NHLBI NIH HHS T32 HL007563NHLBI NIH HHS U10 HL109152NIAID NIH HHS AI-40600NIAID NIH HHS R01 AI040600
6 · The paper itself

Abstract

backgroundSevere asthma remains poorly characterized, although it likely consists of at least 1 phenotype with features of TH2-like inflammation. IL1RL1, encoding both the IL-33 receptor, ST2L, and decoy receptor, sST2, has been genetically associated with asthma, though the mechanism for susceptibility remains unknown.

objectiveGiven previous data supporting a role for IL1RL1 in TH2 inflammation, we hypothesized that ST2L expression might be increased in TH2-like asthma and that expression levels would be associated with single nucleotide polymorphisms in IL1RL1, possibly explaining its genetic relationship with asthma. We also sought to evaluate the regulation of ST2L and sST2 in vitro.

methodsEndobronchial brushings and biopsies were obtained and expression of ST2L compared by severity levels, as well as by TH2-like biomarkers. Subjects were genotyped and the relationship of dichotomous expression of ST2L and sST2 to single nucleotide polymorphisms in IL1RL1 were determined. Epithelial cells were grown in air-liquid interface culture, and ST2L and sST2 responses to IFN-γ and IL-13 were evaluated.

resultsST2L expression was increased in severe asthma (P = .02) and associated with multiple indicators of TH2-like inflammation, including blood eosinophils (P = .001), exhaled nitric oxide (P = .003), and epithelial CLCA1 (P < .0001) and eotaxin-3 (P = .001) mRNA expression. Multiple single nucleotide polymorphisms in IL1RL1 were found in relation to dichotomous expression of both ST2L and sST2. sST2 expression was associated with IFN-γ expression in bronchoalveolar lavage, while inducing its expression in vitro in primary human epithelial cells.

conclusionBoth pathologic and genetic approaches support a role for IL1RL1 in severe asthma, as well as TH2-lke asthma, suggesting that targeting this pathway may have therapeutic benefits.

Indexed as

AsthmaAdultBronchoalveolar Lavage FluidChemokine CCL26Chemokines, CCChloride ChannelsEpithelial CellsFemaleGenotypeHumansInterferon-gammaInterleukin-13Interleukin-1 Receptor-Like 1 ProteinMaleMiddle AgedNitric OxideCCL26 protein, humanChemokine CCL26Chemokines, CCChloride ChannelsCLCA1 protein, humanIL1RL1 protein, humanInterferon-gammaInterleukin-13Interleukin-1 Receptor-Like 1 ProteinNitric OxideReceptors, Cell SurfaceRNA, MessengerAsthmaIL1RL1single nucleotide polymorphismssST2ST2LT(H)2 inflammation

Identifiers

PMID25091434
PMCPMC4289095
OpenAlexW2151306802

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.