Evidence map›Paper›PMID 31626304›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2020

Transcriptional Profiling of the Murine Airway Response to Acute Ozone Exposure.

Adelaide Tovar, Gregory J Smith, Joseph M Thomas, Wesley L Crouse, Jack R Harkema, Samir N P Kelada

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Single-cell transcriptomics reveal alveolar macrophage-specific responses in single-hit ozone exposure model in mice.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Docosahexaenoic Acid and Its Metabolites Protect against Ozone-induced Pulmonary Inflammation.American journal of respiratory cell and molecular biology · 2025
    Article
  9. Article
  10. Evaluating the role of alveolar macrophages in tolerance to ozone.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  11. Article
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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 3 institutions in 1 country.

Adelaide TovarDepartment of Genetics.
Gregory J SmithDepartment of Genetics.
Joseph M ThomasDepartment of Genetics.
Wesley L CrouseDepartment of Genetics.
Jack R HarkemaDepartment of Pathology & Diagnostic Investigation and Institute for Integrated Toxicology, Michigan State University, East Lansing, Michigan 48824.
Samir N P KeladaDepartment of Genetics.
University of North Carolina at Chapel Hill · USMichigan State University · USSociety of Environmental Toxicology and Chemistry · US

Funding

UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Stephanie Engel · 2001 to 2026
$36.3M
TOXICOLOGYT32ES007126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ILONA JASPERS, Bernard E. Weissman · 1985 to 2026
$13.0M
Gene-Environment Interactions with Ozone in Experimental AsthmaR01ES024965 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KELADA, SAMIR · 2015 to 2019
$2.2M
NIEHS NIH HHS P30 ES010126NIEHS NIH HHS R01 ES024965NIEHS NIH HHS T32 ES007126
6 · The paper itself

Abstract

Ambient ozone (O3) exposure has serious consequences on respiratory health, including airway inflammation and injury. Decades of research have yielded thorough descriptions of these outcomes; however, less is known about the molecular processes that drive them. The aim of this study was to further describe the cellular and molecular responses to O3 exposure in murine airways, with a particular focus on transcriptional responses in 2 critical pulmonary tissue compartments: conducting airways (CA) and airway macrophages (AM). After exposing adult, female C57BL/6J mice to filtered air, 1 or 2 ppm O3, we assessed hallmark responses including airway inflammation (cell counts and cytokine secretion) and injury (epithelial permeability), followed by gene expression profiling of CA and AM by RNA-seq. As expected, we observed concentration-dependent increases in airway inflammation and injury. Conducting airways and AM both exhibited changes in gene expression to both 1 and 2 ppm O3 that were largely compartment-specific. In CA, genes associated with epithelial barrier function, detoxification processes, and cellular proliferation were altered, while O3 affected genes involved in innate immune signaling, cytokine production, and extracellular matrix remodeling in AM. Further, CA and AM also exhibited notable differences in concentration-response expression patterns for large numbers of genes. Overall, our study has described transcriptional responses to acute O3 exposure, revealing both shared and unique gene expression patterns across multiple concentrations of O3 and in 2 important O3-responsive tissues. These profiles provide broad mechanistic insight into pulmonary O3 toxicity, and reveal a variety of targets for focused follow-up studies.

Indexed as

Air PollutantsAnimalsBronchoalveolar Lavage FluidFemaleInflammationLungMaleMiceMice, Inbred C57BLOzoneToxicity Tests, AcuteAir PollutantsOzoneair pollutioninflammationinjurylungmouseozonetranscriptomics

Identifiers

PMID31626304
PMCPMC6944221
OpenAlexW2981191564

What OpenQuestion holds

Textmetadata
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.