scRNA-seq of lung cells from murine model of ozone induced asthma exacerbation

Ozone (O3) inhalation triggers asthmatic airway hyperresponsiveness (AHR), but the mechanisms by which this occurs are unknown. Previously, we developed a murine model of dust mite, ragweed, and aspergillus (DRA)-induced allergic lung inflammation followed by O3 exposure for mechanistic investigation. In this model, mice exposed to DRA or O3 alone do not develop AHR, but the two exposures combined have a synergistic effect and the DRA+O3 exposure group develops significant AHR. The present study used single cell RNA-sequencing for unbiased profiling of cells within the lungs of mice exposed to DRA, O3, or DRA+O3, to identify the components that contribute to AHR. Inflammation is generally considered the underlying cause of AHR, so immune cells were of specific focus. Overall design: Lung cells from C57BL/6J mice from 4 different exposure groups (untreated controls, DRA allergen mixture, ozone exposed, and DRA+ozone) were analyzed by scRNA-seq. There are two replicates for each exposure group; 1 male (cells from 3 mice pooled) and 1 female (cells from 3 mice pooled).