Sex Differences in Pulmonary Eicosanoids and Specialized Pro-Resolving Mediators in Response to Ozone Exposure.


Journal

Toxicological sciences : an official journal of the Society of Toxicology
ISSN: 1096-0929
Titre abrégé: Toxicol Sci
Pays: United States
ID NLM: 9805461

Informations de publication

Date de publication:
30 08 2021
Historique:
pubmed: 28 6 2021
medline: 30 9 2021
entrez: 27 6 2021
Statut: ppublish

Résumé

Ozone (O3) is a criteria air pollutant known to increase the morbidity and mortality of cardiopulmonary diseases. This occurs through a pulmonary inflammatory response characterized by increased recruitment of immune cells into the airspace, pro-inflammatory cytokines, and pro-inflammatory lipid mediators. Recent evidence has demonstrated sex-dependent differences in the O3-induced pulmonary inflammatory response. However, it is unknown if this dimorphic response is evident in pulmonary lipid mediator metabolism. We hypothesized that there are sex-dependent differences in lipid mediator production following acute O3 exposure. Male and female C57BL/6J mice were exposed to 1 part per million O3 for 3 h and were necropsied at 6 or 24 h following exposure. Lung lavage was collected for cell differential and total protein analysis, and lung tissue was collected for mRNA analysis, metabololipidomics, and immunohistochemistry. Compared with males, O3-exposed female mice had increases in airspace neutrophilia, neutrophil chemokine mRNA, pro-inflammatory eicosanoids such as prostaglandin E2, and specialized pro-resolving mediators (SPMs), such as resolvin D5 in lung tissue. Likewise, precursor fatty acids (arachidonic and docosahexaenoic acid; DHA) were increased in female lung tissue following O3 exposure compared with males. Experiments with ovariectomized females revealed that loss of ovarian hormones exacerbates pulmonary inflammation and injury. However, eicosanoid and SPM production were not altered by ovariectomy despite depleted pulmonary DHA concentrations. Taken together, these data indicate that O3 drives an increased pulmonary inflammatory and bioactive lipid mediator response in females. Furthermore, ovariectomy increases susceptibility to O3-induced pulmonary inflammation and injury, as well as decreases pulmonary DHA concentrations.

Identifiants

pubmed: 34175951
pii: 6310193
doi: 10.1093/toxsci/kfab081
pmc: PMC8404991
doi:

Substances chimiques

Eicosanoids 0
Ozone 66H7ZZK23N

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

170-183

Subventions

Organisme : NIEHS NIH HHS
ID : P30 ES025128
Pays : United States
Organisme : NCRR NIH HHS
ID : UL1 RR025780
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES020897
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES031378
Pays : United States
Organisme : NIEHS NIH HHS
ID : T32 ES007046
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES027574
Pays : United States
Organisme : NIH HHS
ID : S10 OD010366
Pays : United States

Informations de copyright

© The Author(s) 2021. Published by Oxford University Press on behalf of the Society of Toxicology.All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Auteurs

Michael J Yaeger (MJ)

Pulmonary, Critical Care and Sleep Medicine, Ohio State University Wexner Medical Center, Davis Heart and Lung Research Institute, Columbus, Ohio 43210, USA.

Sky W Reece (SW)

Department of Pharmacology and Toxicology, Brody School of Medicine, East Carolina University, Greenville, North Carolina 27858, USA.

Brita Kilburg-Basnyat (B)

Department of Pharmacology and Toxicology, Brody School of Medicine, East Carolina University, Greenville, North Carolina 27858, USA.

Miles X Hodge (MX)

Department of Pharmacology and Toxicology, Brody School of Medicine, East Carolina University, Greenville, North Carolina 27858, USA.

Anandita Pal (A)

Department of Nutrition, Gillings School of Global Public Health and School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.

Katelyn Dunigan-Russell (K)

Pulmonary, Critical Care and Sleep Medicine, Ohio State University Wexner Medical Center, Davis Heart and Lung Research Institute, Columbus, Ohio 43210, USA.

Bin Luo (B)

Department of Pharmacology and Toxicology, Brody School of Medicine, East Carolina University, Greenville, North Carolina 27858, USA.

Dorothy J You (DJ)

Department of Biological Sciences, North Carolina State University, Raleigh, North Carolina 27107, USA.

James C Bonner (JC)

Department of Biological Sciences, North Carolina State University, Raleigh, North Carolina 27107, USA.

Espen E Spangenburg (EE)

Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, North Carolina 27858, USA.

Debra Tokarz (D)

Experimental Pathology Laboratories, Inc., Research Triangle Park, North Carolina 27709, USA.

Johanna Hannan (J)

Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, North Carolina 27858, USA.

Michael Armstrong (M)

Department of Pharmaceutical Sciences, University of Colorado-AMC, Aurora, Colorado 80045, USA.

Jonathan Manke (J)

Department of Pharmaceutical Sciences, University of Colorado-AMC, Aurora, Colorado 80045, USA.

Nichole Reisdorph (N)

Department of Pharmaceutical Sciences, University of Colorado-AMC, Aurora, Colorado 80045, USA.

Robert M Tighe (RM)

Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA.

S Raza Shaikh (SR)

Department of Nutrition, Gillings School of Global Public Health and School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.

Kymberly M Gowdy (KM)

Pulmonary, Critical Care and Sleep Medicine, Ohio State University Wexner Medical Center, Davis Heart and Lung Research Institute, Columbus, Ohio 43210, USA.

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Classifications MeSH