Evidence map›Paper›PMID 28652606›Full record

ArticleScientific reports2017

Interleukin 33 exacerbates antigen driven airway hyperresponsiveness, inflammation and remodeling in a mouse model of asthma.

L C Sjöberg, A Zoltowska Nilsson, Y Lei, J A Gregory, M Adner, G P Nilsson

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 74 citations in OpenAlex.

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  17. IL-33/Regulatory T-Cell Axis Suppresses Skin Fibrosis.The Journal of investigative dermatology · 2022
    Article
  18. Review
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  20. IL-1β Promotes Expansion of IL-33American journal of respiratory cell and molecular biology · 2022
    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

6 authors at 2 institutions in 1 country.

L C SjöbergUnit of Experimental Asthma and Allergy Research, Institute of Environmental Medicine, Karolinska University Hospital, Stockholm, Sweden.
A Zoltowska NilssonImmunology and Allergy Unit, Department of Medicine, Karolinska University Hospital, Stockholm, Sweden.
Y LeiImmunology and Allergy Unit, Department of Medicine, Karolinska University Hospital, Stockholm, Sweden.
J A GregoryUnit of Experimental Asthma and Allergy Research, Institute of Environmental Medicine, Karolinska University Hospital, Stockholm, Sweden.
M AdnerUnit of Experimental Asthma and Allergy Research, Institute of Environmental Medicine, Karolinska University Hospital, Stockholm, Sweden.
G P NilssonImmunology and Allergy Unit, Department of Medicine, Karolinska University Hospital, Stockholm, Sweden. Gunnar.P.Nilsson@ki.se.
Karolinska University Hospital · SEKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin 33 (IL-33) represents a potential link between the airway epithelium and induction of Th2-type inflammatory responses associated with the development of asthma. This study investigated the potential of IL-33 to exacerbate antigen driven asthma responses. An ovalbumin (OVA) asthma model was used in which sensitized C57BL/6 mice were exposed to IL-33 before each OVA challenge. IL-33 given to sensitized mice acted synergistically with antigen and aggravated airway inflammation, hyperresponsiveness and remodeling compared with mice that were only OVA sensitized and challenged and mice that were only exposed to IL-33. Elevated levels of local and systemic mast cell protease mMCP-1, as well as antigen-specific IgE production, were observed following IL-33 administration to sensitized mice. Similarly, exposing OVA-sensitized mice to IL-33 increased the Th2 cytokine levels, including IL-4, IL-5 and IL-13. Furthermore, IL-33 and OVA administration to OVA-sensitized mice increased ILC2s in the lung, suggesting a role for ILC2s in IL-33-mediated exacerbation of OVA-induced airway responses. Collectively, these findings show that IL-33 aggravates important features of antigen-driven asthma, which may have implications for asthma exacerbations.

Indexed as

Airway RemodelingAnimalsAsthmaBronchoalveolar Lavage FluidDisease Models, AnimalInflammationInterleukin-33LungMaleMice, Inbred C57BLOvalbuminRespiratory HypersensitivityInterleukin-33Ovalbumin

Identifiers

PMID28652606
PMCPMC5484710
OpenAlexW2651239463

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.