Evidence map›Paper›PMID 24365139›Full record

ArticleThe Journal of allergy and clinical immunology2014

A mouse model links asthma susceptibility to prenatal exposure to diesel exhaust.

Sarah Manners, Rafeul Alam, David A Schwartz, Magdalena M Gorska

Open access · greenAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
7.0field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 106 citations in OpenAlex.

  1. Early Life Exposure to Air Pollutants and Childhood Asthma.Current allergy and asthma reports · 2026
    Review
  2. Article
  3. Update on environmental determinants of allergic diseases.The Journal of allergy and clinical immunology · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Maternal Allergen Exposures and Development of Asthma: Kids Are Airways Nervy.American journal of respiratory cell and molecular biology · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Airborne Benzo[a]Pyrene may contribute to divergent Pheno-Endotypes in children.Environmental health : a global access science source · 2021
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Sarah MannersDepartment of Medicine, Division of Allergy and Clinical Immunology, National Jewish Health, Denver, Colo.
Rafeul AlamDepartment of Medicine, Division of Allergy and Clinical Immunology, National Jewish Health, Denver, Colo; Department of Medicine, Division of Allergy and Clinical Immunology, University of Colorado Denver, Aurora, Colo.
David A SchwartzDepartment of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Denver, Aurora, Colo.
Magdalena M GorskaDepartment of Medicine, Division of Allergy and Clinical Immunology, National Jewish Health, Denver, Colo; Department of Medicine, Division of Allergy and Clinical Immunology, University of Colorado Denver, Aurora, Colo. Electronic address: gorskam@njhealth.org.
University of Colorado Denver · US

Funding

Colorado Clinical and Translational Sciences InstituteUL1TR001082 · NCATS · UNIVERSITY OF COLORADO DENVER · PI SOKOL, RONALD J. · 2013 to 2017
$48.0M
Project 3: Environmental Determinants of Host DefenseP01ES018181 · NIEHS · NATIONAL JEWISH HEALTH · PI SCHWARTZ, DAVID ALBERT · 2009 to 2013
$5.7M
Asthma susceptibility due to environmental programming of innate immunity in uteroR01HL122995 · NHLBI · NATIONAL JEWISH HEALTH · PI GORSKA, MAGDALENA MARIA · 2015 to 2024
$5.2M
Colorado Clinical and Translational Sciences InstituteKL2TR001080 · NCATS · UNIVERSITY OF COLORADO DENVER · PI SOKOL, RONALD J. · 2013 to 2017
$2.6M
Role of MEK1 in T cell function in asthmaR01AI091614 · NIAID · NATIONAL JEWISH HEALTH · PI ALAM, RAFEUL · 2011 to 2015
$2.0M
Sprouty-2 Regulation of Signaling in AsthmaR01AI102943 · NIAID · NATIONAL JEWISH HEALTH · PI ALAM, RAFEUL · 2014 to 2017
$1.6M
Colorado Clinical and Translational Science Institute (KL2)KL2TR000156 · NCATS · UNIVERSITY OF COLORADO DENVER · PI SOKOL, RONALD J. · 2012 to 2013
$521k
NCATS NIH HHS CTSI KL2 TR000156NCATS NIH HHS KL2 TR000156NCATS NIH HHS KL2 TR001080NCATS NIH HHS UL1 TR001082NHLBI NIH HHS R01 HL122995NIAID NIH HHS R01 AI091614NIAID NIH HHS R01 AI102943NIEHS NIH HHS P01 ES-018181NIEHS NIH HHS P01 ES018181
6 · The paper itself

Abstract

backgroundMost asthma begins in the first years of life. This early onset cannot be attributed merely to genetic factors because the prevalence of asthma is increasing. Epidemiologic studies have indicated roles for prenatal and early childhood exposures, including exposure to diesel exhaust. However, little is known about the mechanisms. This is largely due to a paucity of animal models.

objectiveWe aimed to develop a mouse model of asthma susceptibility through prenatal exposure to diesel exhaust.

methodsPregnant C57BL/6 female mice were given repeated intranasal applications of diesel exhaust particles (DEPs) or PBS. Offspring underwent suboptimal immunization and challenge with ovalbumin (OVA) or received PBS. Pups were examined for features of asthma; lung and liver tissues were analyzed for transcription of DEP-regulated genes.

resultsOffspring of mice exposed to DEPs were hypersensitive to OVA, as indicated by airway inflammation and hyperresponsiveness, increased serum OVA-specific IgE levels, and increased pulmonary and systemic TH2 and TH17 cytokine levels. These cytokines were primarily produced by natural killer (NK) cells. Antibody-mediated depletion of NK cells prevented airway inflammation. Asthma susceptibility was associated with increased transcription of genes known to be specifically regulated by the aryl hydrocarbon receptor and oxidative stress. Features of asthma were either marginal or absent in OVA-treated pups of PBS-exposed mice.

conclusionWe created a mouse model that linked maternal exposure to DEPs with asthma susceptibility in offspring. Development of asthma was dependent on NK cells and associated with increased transcription from aryl hydrocarbon receptor- and oxidative stress-regulated genes.

Indexed as

Air PollutantsAnimalsAsthmaBronchial HyperreactivityDisease Models, AnimalDisease SusceptibilityFemaleGene Expression ProfilingGene Expression RegulationHumansImmunoglobulin EInterleukin-17Killer Cells, NaturalMaternal ExposureMiceMice, Inbred C57BLAir PollutantsImmunoglobulin EInterleukin-17OvalbuminReceptors, Aryl HydrocarbonVehicle Emissionsaryl hydrocarbon receptorasthmadiesel exhaust particlesIL-13IL-17IL-5mouse modelnatural killer cellsPrenatal exposure

Identifiers

PMID24365139
PMCPMC4065237
OpenAlexW2044740886

What OpenQuestion holds

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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.