Data from: Transcriptional profiling of the murine airway response to acute ozone exposure

Ambient ozone (O3) exposure has serious consequences on respiratory
health, including airway inflammation and injury. Decades of research have
yielded thorough descriptions of these outcomes; however, less is known
about the molecular processes that drive them. The aim of this study was
to further describe the cellular and molecular responses to O3 exposure in
murine airways, with a particular focus on transcriptional responses in
two critical compartments: conducting airways (CA) and airway macrophages
(AM). After exposing adult, female C57BL/6J mice to filtered air, 1 or 2
ppm O3, we assessed hallmark responses including airway inflammation (cell
counts and cytokine secretion) and injury (epithelial permeability),
followed by gene expression profiling of CA and AM by RNA-seq. As
expected, we observed concentration-dependent increases in airway
inflammation and injury. CA and AM both exhibited changes in gene
expression to both 1 and 2 ppm O3 that were largely compartment-specific.
In CA, genes associated with epithelial barrier function, detoxification
processes, and cellular proliferation were altered, while O3 affected
genes involved in innate immune signaling, cytokine production, and
extracellular matrix remodeling in AM. Further, CA and AM also exhibited
notable differences in concentration-response expression patterns for
large numbers of genes. Overall, our study has described transcriptional
responses to acute O3 exposure, revealing both shared and unique gene
expression patterns across multiple concentrations of O3 and in two
important O3-responsive tissues. These profiles provide broad mechanistic
insight into pulmonary O3 toxicity, and reveal a variety of targets for
focused follow-up studies.