Evidence map›Paper›PMID 29247675›Full record

ArticleToxicology and applied pharmacology2018

Adrenergic and glucocorticoid receptor antagonists reduce ozone-induced lung injury and inflammation.

Andres R Henriquez, Samantha J Snow, Mette C Schladweiler, Colette N Miller, Janice A Dye, Allen D Ledbetter, Judy E Richards, Kevin Mauge-Lewis, Marie A McGee, Urmila P Kodavanti

Abstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed, 60 citations in OpenAlex.

  1. Trial
  2. Review
  3. Estrogen and glucocorticoid receptors co-regulate acrolein-induced respiratory and systemic homeostatic stress responses.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Neuroendocrine contribution to sex-related variations in adverse air pollution health effects.Journal of toxicology and environmental health. Part B, Critical reviews · 2024
    Review
  9. Review
  10. Individual and joint effects of prenatal PMEnvironmental research · 2024
    Article
  11. Article
  12. Association between prenatal and childhood PMEnvironmental epidemiology (Philadelphia, Pa.) · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  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 3 institutions in 1 country.

Andres R HenriquezCurriculum in Toxicology, University of North Carolina-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.
Mette C SchladweilerEnvironmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC, United States.
Colette N MillerEnvironmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC, United States.
Janice A DyeEnvironmental 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.
Judy E RichardsEnvironmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC, United States.
Kevin Mauge-LewisCurriculum in Toxicology, University of North Carolina-Chapel Hill, Chapel Hill, NC, United States.
Marie A McGeeOak Ridge Institute for Science and Education, Oak Ridge, TN, 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 · USUniversity of North Carolina at Chapel Hill · USOak Ridge Associated Universities · 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

Recent studies showed that the circulating stress hormones, epinephrine and corticosterone/cortisol, are involved in mediating ozone-induced pulmonary effects through the activation of the sympathetic-adrenal-medullary (SAM) and hypothalamus-pituitary-adrenal (HPA) axes. Hence, we examined the role of adrenergic and glucocorticoid receptor inhibition in ozone-induced pulmonary injury and inflammation. Male 12-week old Wistar-Kyoto rats were pretreated daily for 7days with propranolol (PROP; a non-selective β adrenergic receptor [AR] antagonist, 10mg/kg, i.p.), mifepristone (MIFE; a glucocorticoid receptor [GR] antagonist, 30mg/kg, s.c.), both drugs (PROP+MIFE), or respective vehicles, and then exposed to air or ozone (0.8ppm), 4h/d for 1 or 2 consecutive days while continuing drug treatment. Ozone exposure alone led to increased peak expiratory flow rates and enhanced pause (Penh); with greater increases by day 2. Receptors blockade minimally affected ventilation in either air- or ozone-exposed rats. Ozone exposure alone was also associated with marked increases in pulmonary vascular leakage, macrophage activation, neutrophilic inflammation and lymphopenia. Notably, PROP, MIFE and PROP+MIFE pretreatments significantly reduced ozone-induced pulmonary vascular leakage; whereas PROP or PROP+MIFE reduced neutrophilic inflammation. PROP also reduced ozone-induced increases in bronchoalveolar lavage fluid (BALF) IL-6 and TNF-α proteins and/or lung Il6 and Tnfα mRNA. MIFE and PROP+MIFE pretreatments reduced ozone-induced increases in BALF N-acetyl glucosaminidase activity, and lymphopenia. We conclude that stress hormones released after ozone exposure modulate pulmonary injury and inflammatory effects through AR and GR in a receptor-specific manner. Individuals with pulmonary diseases receiving AR and GR-related therapy might experience changed sensitivity to air pollution.

Indexed as

Adrenergic beta-AntagonistsAnimalsBronchoalveolar Lavage FluidHormone AntagonistsInflammationInflammation MediatorsLung InjuryMaleMifepristoneOzoneRatsRats, Inbred WKYReceptors, AdrenergicReceptors, GlucocorticoidAdrenergic beta-AntagonistsHormone AntagonistsInflammation MediatorsMifepristoneOzoneReceptors, AdrenergicReceptors, GlucocorticoidAdrenergic receptor antagonistGlucocorticoid receptor antagonistLung inflammationLung injuryOzoneStress response

Identifiers

PMID29247675
PMCPMC7110430
OpenAlexW2773105336

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.