β₂-Adrenoceptor signaling in airway epithelial cells promotes eosinophilic inflammation, mucous metaplasia, and airway contractility.

ABSTRACT: The mostly widely used bronchodilators in asthma therapy are β₂-adrenoreceptor (β₂AR) agonists, but their chronic use causes paradoxical adverse effects. We have previously determined that β₂AR activation is required for expression of the asthma phenotype in mice, but the cell types involved are unknown. We now demonstrate that β₂AR signaling in the airway epithelium is sufficient to mediate key features of the asthmatic responses to IL-13 in murine models. Our data show that inhibition of β₂AR signaling with an aerosolized antagonist attenuates airway hyperresponsiveness (AHR), eosinophilic inflammation, and mucus-production responses to IL-13, whereas treatment with an aerosolized agonist worsens these phenotypes, suggesting that β

SUBMITTER: Nguyen LP 

PROVIDER: S-EPMC5664525 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature