Evidence map›Paper›PMID 28623178›Full record

ArticleToxicology and applied pharmacology2017

Adrenal-derived stress hormones modulate ozone-induced lung injury and inflammation.

Andres Henriquez, John House, Desinia B Miller, Samantha J Snow, Anna Fisher, Hongzu Ren, Mette C Schladweiler, Allen D Ledbetter, Fred Wright, Urmila P Kodavanti

Open access · greenAbstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

35 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Neuroendocrine contribution to sex-related variations in adverse air pollution health effects.Journal of toxicology and environmental health. Part B, Critical reviews · 2024
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Aerosol physicochemical determinants of carbon black and ozone inhalation co-exposure induced pulmonary toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Scavenger Receptor BI Attenuates IL-17A-Dependent Neutrophilic Inflammation in Asthma.American journal of respiratory cell and molecular biology · 2021
    Article
  16. The Role of Hepatic Vagal Tone in Ozone-Induced Metabolic Dysfunction in the Liver.Toxicological sciences : an official journal of the Society of Toxicology · 2021
    Article
  17. Article
  18. Article
  19. 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

10 authors at 4 institutions in 1 country.

Andres HenriquezCurriculum in Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.
John HouseBioinformatics Research Center, North Carolina State University, Raleigh, NC, United States.
Desinia B MillerCurriculum in Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.
Samantha J SnowEnvironmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC, United States.
Anna FisherResearch Cores Unit, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC, United States.
Hongzu RenResearch Cores Unit, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC, United States.
Mette C SchladweilerEnvironmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC, United States.
Allen D LedbetterEnvironmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC, United States.
Fred WrightBioinformatics Research Center, North Carolina State University, Raleigh, NC, United States.
Urmila P KodavantiEnvironmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC, United States. Electronic address: kodavanti.urmila@epa.gov.
Environmental Protection Agency · USResearch Triangle Park Foundation · USNorth Carolina State University · USUniversity of North Carolina at Chapel Hill · US

Funding

TOXICOLOGYT32ES007126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ILONA JASPERS, Bernard E. Weissman · 1985 to 2026
$13.0M
Intramural EPA EPA999999NIEHS NIH HHS T32 ES007126
6 · The paper itself

Abstract

Ozone-induced systemic effects are modulated through activation of the neuro-hormonal stress response pathway. Adrenal demedullation (DEMED) or bilateral total adrenalectomy (ADREX) inhibits systemic and pulmonary effects of acute ozone exposure. To understand the influence of adrenal-derived stress hormones in mediating ozone-induced lung injury/inflammation, we assessed global gene expression (mRNA sequencing) and selected proteins in lung tissues from male Wistar-Kyoto rats that underwent DEMED, ADREX, or sham surgery (SHAM) prior to their exposure to air or ozone (1ppm), 4h/day for 1 or 2days. Ozone exposure significantly changed the expression of over 2300 genes in lungs of SHAM rats, and these changes were markedly reduced in DEMED and ADREX rats. SHAM surgery but not DEMED or ADREX resulted in activation of multiple ozone-responsive pathways, including glucocorticoid, acute phase response, NRF2, and PI3K-AKT. Predicted targets from sequencing data showed a similarity between transcriptional changes induced by ozone and adrenergic and steroidal modulation of effects in SHAM but not ADREX rats. Ozone-induced increases in lung Il6 in SHAM rats coincided with neutrophilic inflammation, but were diminished in DEMED and ADREX rats. Although ozone exposure in SHAM rats did not significantly alter mRNA expression of Ifnγ and Il-4, the IL-4 protein and ratio of IL-4 to IFNγ (IL-4/IFNγ) proteins increased suggesting a tendency for a Th2 response. This did not occur in ADREX and DEMED rats. We demonstrate that ozone-induced lung injury and neutrophilic inflammation require the presence of circulating epinephrine and corticosterone, which transcriptionally regulates signaling mechanisms involved in this response.

Indexed as

OzoneStress, PhysiologicalAdrenal CortexAdrenalectomyAdrenal MedullaAnimalsCorticosteroneCytokinesDisease Models, AnimalEpinephrineGene Expression RegulationInflammation MediatorsLungLung InjuryMaleNeutrophilsCorticosteroneCytokinesEpinephrineInflammation MediatorsOzoneRNA, MessengerAdrenalectomyLungOzoneRNAseqStress hormones

Identifiers

PMID28623178
PMCPMC6757346
OpenAlexW2625597193

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.