Inhaled fluticasone and salmeterol suppress eosinophilic airway inflammation in chronic obstructive pulmonary disease: relations with lung function and bronchodilator reversibility

The aim of this study was to determine whether combined inhaled corticosteroids and long-acting beta(2) agonists can suppress eosinophilic inflammation in chronic dostructive plumonary disease (COPD) and to investigate the association between the level of eosinophilia and the degree of bronchodilator reversibility. Sixty-two patients with stable COPD (forced expiratory volume in 1 [FEV(1)] of 30%-70% predicted before bronchodilation) were enrolled from our outpatient clinic. Patients received inhaled fluticasone (100 microg)/salmeterol (50 microg) twice daily for two months. Lung function measurements, bronchodilator tests, and sputum induction were performed. The number of inflammatory cells and mediators, including interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha), and eosinophilic cationic protein (ECP), were measured. Treatment with inhaled fluticasone and salmeterol significantly suppressed eosinophilic inflammation in COPD patients with sputum eosinophilia (mean 8.9% +/- 2.0% vs. 1.6% +/- 0.5%, p = 0.003), but insignificant differences in FEV(1) and FVC between patients with and without eosinophilia suggested that suppression of eosinophilic inflammation had no effect on FEV(1) or FVC. Reduction in the percentage of eosinophils was significantly correlated with decreased levels of ECP (r = 0.48, p < 0.001). Levels of neutrophils, IL-8, and TNF-alpha were not affected. Sputum eosinophilia was not related to the degree of bronchodilator reversibility. The degree of bronchodilator reversibility did not predict the increase in FEV(1) and FVC after treatment with inhaled corticosteroids/long-acting beta(2) agonists. Suppression of eosinophilic inflammation and bronchodilator responsiveness indices were not correlated with clinical outcomes in COPD patients treated with inhaled corticosteroids/long-acting beta(2) agonists.