Effect of Procaterol, a?2 Selective Adrenergic Receptor Agonist, on Airway Inflammation and

Background: β-agonists are frequently used as bronchodilators for asthma as not only a reliever but also a controller, and their utility has increased with the development of long-acting β2 selective drugs. Although anti-inflammatory effects of β2 selective-agonists have been reported in vitro, side effects on augmentation of air-way hyperresponsiveness by chronic use of β2 selective-agonists have been described in several reports. In this study, we investigated the effects of procaterol, a second-generation β2-agonist, on airway inflammation in vivo using an antigen-specific murine model of asthma. Methods: Mice immunized with ovalbumin (OVA) + alum and challenged with inhaled ovalbumin were orally administered procaterol during the challenge. After inhalation, the mice were tracheostomized and placed in a body box under controlled ventilation to measure airway resistance before and after acetylcholine inhalation. Results: Administration of procaterol at a clinical dose equivalent did not augment airway hyperresponsive-ness, inflammation of the airway wall, or subsequent airway wall thickening induced by OVA inhalation. BALF cell analysis revealed that the eosinophil number in the BALF was significantly reduced in procaterol-treated mice compared to untreated mice. Conclusions: Oral administration of procaterol at a clinical dose did not augment airway responsiveness, but did reduce eosinophil inflammation. KEY WORDS airway hyperresponsiveness, allergic inflammation, eosinophil, murine model, β2 adrenergic receptor agonis