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• W2949778511 abstract "Abstract Exposure to ambient ozone (O 3 ) pollution causes airway inflammation, epithelial injury, and decreased lung function. Long-term exposure is associated with increased mortality and exacerbations of respiratory conditions. While the adverse health effects of O 3 exposure have been thoroughly described, less is known about the molecular processes that drive these outcomes. The aim of this study was to describe the cellular and molecular alterations observed in murine airways after exposure to either 1 or 2 ppm O 3 . After exposing adult, female C57BL/6J mice to filtered air, 1 or 2 ppm O 3 for 3 hours, we assessed hallmark responses including airway inflammatory cell counts, epithelial permeability, cytokine secretion, and morphological alterations of the large airways. Further, we performed RNA-seq to profile gene expression in two critical tissues involved in O 3 responses: conducting airways (CA) and airway macrophages (AM). We observed a concentration-dependent increase in airway inflammation and injury, and a large number of genes were differentially expressed in both target tissues at both concentrations of O 3 . Genes that were differentially expressed in CA were generally associated with barrier function, detoxification processes, and cellular proliferation. The differentially expressed genes in AM were associated with innate immune signaling, cytokine production, and extracellular matrix remodeling. Overall, our study has described transcriptional responses to acute O 3 exposure, revealing both shared and unique gene expression patterns across multiple concentrations of O 3 and in two important O 3 -responsive tissues. These profiles provide broad mechanistic insight into pulmonary O 3 toxicity, and reveal a variety of targets for refined follow-up studies." @default.
• W2949778511 created "2019-06-27" @default.
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• W2949778511 date "2019-06-05" @default.
• W2949778511 modified "2023-09-28" @default.
• W2949778511 title "Transcriptional profiling of the murine airway response to acute ozone exposure" @default.
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• W2949778511 doi "https://doi.org/10.1101/660316" @default.
• W2949778511 hasPublicationYear "2019" @default.
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