Cigarette smoking, the major cause of chronic obstructive pulmonary disease (COPD), induces activation of pro-inflammatory pathways in the airway epithelium. Salbutamol, a selective and short-acting β2-adrenoceptor agonist, is used for bronchospasm relief in patients with asthma and COPD. In addition, salbutamol also present anti-inflammatory effects. Here, we evaluated whether salbutamol (10-5-10- 7 M) can reduce on bronchial epithelial cells (BEAS-2B cells) the inflammatory parameters induced by cigarette smoke extract (CSE; 1%). After 24h, Salbutamol reduced the IL-1β production induced by CSE in a concentration-response manner. Salbutamol (10-6 M) reduced the IL-8 production and increased the IL-10 production on CSE-stimulated cells. In addition, salbutamol (10-6 M) decreased the ICAM-1 expression and the reactive oxygen species production. These anti-inflammatory effects could be associated with the down regulation of activation of NF-κB. Salbutamol may be a potential alternative treatment to airway inflammation caused by cigarette smoking such as in COPD patients.

No abstract