Evidence map›Paper›PMID 31988179›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2020

Endogenous IL-33 and Its Autoamplification of IL-33/ST2 Pathway Play an Important Role in Asthma.

Jenna M Magat, Joanna L Thomas, Justin P Dumouchel, Fiona Murray, Willis X Li, Jinghong Li

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 35 citations in OpenAlex.

  1. Synbiotic Combination ofJournal of microbiology and biotechnology · 2026
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  10. Resolution Potential of Necrotic Cell Death Pathways.International journal of molecular sciences · 2022
    Review
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  15. Molecular hydrogen alleviates asthma through inhibiting IL-33/ILC2 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Article
  16. 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.

Jenna M MagatDepartment of Medicine, University of California San Diego, La Jolla, CA 92093; and.
Joanna L ThomasVeterans Affairs San Diego Healthcare System, San Diego, CA 92093.ORCID 0000-0002-1358-3167
Justin P DumouchelDepartment of Medicine, University of California San Diego, La Jolla, CA 92093; and.
Fiona MurrayDepartment of Medicine, University of California San Diego, La Jolla, CA 92093; and.ORCID 0000-0002-5572-4810
Willis X LiDepartment of Medicine, University of California San Diego, La Jolla, CA 92093; and.ORCID 0000-0001-9041-7341
Jinghong LiDepartment of Medicine, University of California San Diego, La Jolla, CA 92093; and jinghongli@ucsd.edu.ORCID 0000-0003-2497-9295
University of California San Diego · USVA San Diego Healthcare System · US

Funding

Training in the Next Generation in Respiratory ScienceT32HL134632 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MALHOTRA, ATUL, POWELL, FRANK L. · 2017 to 2021
$2.1M
Training in Respiratory Biology: Innovate, Integrate, and TranslateT32HL098062 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI POWELL, FRANK L. · 2010 to 2014
$2.1M
NHLBI NIH HHS T32 HL098062NHLBI NIH HHS T32 HL134632
6 · The paper itself

Abstract

IL-33 and its receptor ST2 are contributing factors to airway inflammation and asthma exacerbation. The IL-33/ST2 signaling pathway is involved in both the onset and the acute exacerbations of asthma. In this study, we address the role of endogenous IL-33 and its autoamplification of the IL-33/ST2 pathway in Ag-dependent and Ag-independent asthma-like models. Wild-type, IL-33 knockout, ST2 knockout mice were either intratracheally administrated with 500 ng of rIL-33 per day for four consecutive days or were sensitized and challenged with OVA over 21 d. In wild-type mice, IL-33 or OVA induced similar airway hyperresponsiveness and eosinophilic airway inflammation. IL-33 induced its own mRNA and ST2L mRNA expression in the lung. IL-33 autoamplified itself and ST2 protein expression in airway epithelial cells. OVA also induced IL-33 and ST2 protein expression. In IL-33 knockout mice, the IL-33- and OVA-induced airway hyperresponsiveness and eosinophilic airway inflammation were both significantly attenuated, whereas IL-33-induced ST2L mRNA expression was preserved, although no autoamplification of IL-33/ST2 pathway was observed. In ST2 knockout mice, IL-33 and OVA induced airway hyperresponsiveness and eosinophilic airway inflammation were both completely diminished, and no IL-33/ST2 autoamplification was observed. These results suggest that endogenous IL-33 and its autoamplification of IL-33/ST2 pathway play an important role in the induction of asthma-like phenotype. Thus an intact IL-33/ST2 pathway is necessary for both Ag-dependent and Ag-independent asthma-like mouse models.

Indexed as

AllergensAnimalsAsthmaBronchoalveolar Lavage FluidDisease Models, AnimalEosinophilsEpithelial CellsHumansInterleukin-1 Receptor-Like 1 ProteinInterleukin-33MiceMice, KnockoutOvalbuminRecombinant ProteinsRespiratory MucosaSignal TransductionAllergensIl1rl1 protein, mouseIl33 protein, mouseInterleukin-1 Receptor-Like 1 ProteinInterleukin-33OvalbuminRecombinant Proteins

Identifiers

PMID31988179
PMCPMC7065953
OpenAlexW3003977192

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.