Evidence map›Paper›PMID 31922608›Full record

ArticleAllergy2020

IL33 contributes to diesel pollution-mediated increase in experimental asthma severity.

Eric B Brandt, Paige E Bolcas, Brandy P Ruff, Gurjit K Khurana Hershey

Open access · greenAbstract read
In one paragraph

Article in Allergy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
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  5. Article
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  7. Review
  8. Frequent exacerbator-a novel endotype of pediatric asthma.The Journal of allergy and clinical immunology · 2025
    Review
  9. The role of mTOR activation in steroid-resistant asthma: insights from particulate matter-induced mouse model and patient studies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Severe Asthmatic Responses: The Impact of TSLP.International journal of molecular sciences · 2023
    Review
  17. Review
  18. The "epiTet" of Air Pollution: Epigenetic Regulation of Airway Inflammation by Tet1.International archives of allergy and immunology · 2023
    Article
  19. DEPs Induce Local Ige Class Switching Independent of Their Ability to Stimulate iBALT de Novo Formation.International journal of environmental research and public health · 2022
    Article
  20. 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

4 authors at 2 institutions in 1 country.

Eric B BrandtDivision of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Paige E BolcasDivision of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Brandy P RuffDivision of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Gurjit K Khurana HersheyDivision of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati Medical Center · US

Funding

TSLP, IL-9-producing mucosal mast cells, and allergic inflammationU19AI070235 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI Gurjit K. Khurana Hershey · 2006 to 2026
$31.3M
Role and Regulation of TSLP in Childhood Allergic DiseaseR01AI127392 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI KHURANA HERSHEY, GURJIT K. · 2018 to 2022
$3.8M
NIAID NIH HHS R01 AI127392NIAID NIH HHS U19 AI070235
6 · The paper itself

Abstract

backgroundExposure to traffic pollution, notably diesel exhaust particles (DEP), increases risk for asthma and asthma exacerbations. The contribution of cytokines generated by stressed lung epithelial cells (IL25, IL33, TSLP) to DEP-induced asthma severity remains poorly understood.

methodsBALB/c mice were exposed intratracheally once to DEP or 9 times over 3-weeks to either saline, DEP, and/or house dust mite extract (HDM). Airway hyper-responsiveness (AHR), pulmonary inflammation, and T-cell subsets were assessed 24 hours after the last exposure in mice sufficient and deficient for the IL33 receptor ST2.

resultsDEP exposure induces oxidative stress, IL6, neutrophils and pulmonary accumulation of IL33, but not IL25 or TSLP or other features of allergic disease. When mice are co-exposed to DEP and low doses of HDM, DEP increases IL33 lung levels and Th2 responses. ST2 deficiency partially protected mice from HDM + DEP induced AHR in association with decreased type 2 inflammation and lung levels of IL5

conclusionIL33 contributes to DEP mediated increase in allergen-induced Th2 inflammation and AHR in a mouse model of severe steroid resistant asthma, potentially through the accumulation of pathogenic IL5

Indexed as

AsthmaRespiratory HypersensitivityAnimalsCytokinesDisease Models, AnimalInterleukin-33LungMiceMice, Inbred BALB CPyroglyphidaeTh2 CellsCytokinesIl33 protein, mouseInterleukin-33diesel exhaust particleshouse dust miteIL33steroid resistant asthmatraffic pollution

Identifiers

PMID31922608
PMCPMC7347449
OpenAlexW2999615329

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.