Methods: Children with asthma underwent bronchoscopy to evaluate refractory wheeze or suspected structural anomalies and grouped according to the level of asthma control by the cACT (childhood asthma control test). Fresh EpC were obtained via endobronchial brushings and cultured in the absence or presence of a physiological concentration of dexamethasone (10-9M) and alterations in gene expression expressed via quantitative PCR.
Results: Baseline expression of CLCA1 but not periostin or SerB2 was higher (p = 0.04) in children with poorly- versus well controlled asthma. Dexamethasone inhibited the expression of the three IL-13 inducible gene signature products in controlled but not poorly-controlled children with asthma.
Conclusions: In children with controlled asthma, bronchial EpCs demonstrated CCS-mediated inhibition of the IL-13-inducible gene signature SerB2, CLCA1, and periostin. In contrast, EpC from poorly-controlled asthmatics failed to show this response. Severe, poorly-controlled asthma reflects in part corticosteroid non-responsiveness of bronchial epithelial cells.