Journal
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
Volume 86, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.etap.2021.103662
Keywords
Ozone; Glucocorticoid; Alveolar macrophage; Inflammation; Polarization; Phagocytosis
Funding
- Health Canada through the Clean Air Regulatory Agenda
- Addressing Air Pollution Horizontal Initiative
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Research shows that different rat strains have varying stress responses to O3 and differences in lung corticosterone levels, which in turn affect the inflammatory gene response of macrophages.
Although considerable inter-individual variability exists in health effects associated with air pollutant exposure, underlying reasons remain unclear. We examined whether innate differences in stress axis function modify lung glucocorticoid and macrophage responses to ozone (O3). Highly-stress responsive Fischer (F344) and less responsive Lewis (LEW) rats were exposed for 4 h by nose-only inhalation to air or O3 (0.8 ppm). Ozone increased corticosterone recovered by bronchoalveolar lavage in both strains (F344 > LEW). Higher corticosterone in F344 was associated with a blunted response to O3 of macrophage pro-inflammatory genes compared to LEW. Pharmacological inhibition of O3-dependent corticosterone production in F344 enhanced the inflammatory gene response to O3, mimicking the LEW phenotype. Examination of potential impacts of glucocorticoids on macrophage function using a human monocyte-derived macrophage cell line (THP-1) showed that cortisol modified phagocytosis in a macrophage phenotype-dependent manner. Overall, our data implicate endogenous glucocorticoids in the regulation of pulmonary macrophage responses to O3.
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