부산대학교 도서관

A previous study suggested that the long-acting β2-adrenergic agonist salmeterol (SM) had inhibitory effects on bronchial mucosal inflammation 6 hours after allergen exposure. To further evaluate the influence of SM on allergen-induced airway inflammation. We studied, in a randomized, double-blind, cross-over trial, 16 mild asthmatic patients who had a dual asthmatic response to allergen inhalation. Subjects received 50 µg of SM or placebo (P), twice daily for 1 week each, separated by a 2-week wash-out period. At the end of each treatment period, after withholding SM for 24 h, they had a methacholine inhalation test (medication was resumed after the test), followed 24 h later by an AC with the concentration of allergen that had induced a LAR at baseline. Airway inflammation was assessed 24 h after the AC by bronchoalveolar lavage (BAL) (n = 16) and bronchial biopsies (n = 13). As expected, SM improved baseline FEV1 and PC20 (P ≤ 0.009) and decreased the allergen-induced early bronchoconstrictive response. There were no significant differences in BAL cell counts after the two treatments. On bronchial biopsies, numbers (median, mm2) of submucosal CD45 (P: 43 ± 23; SM: 161 ± 43, P = 0.031), CD45Ro (P: 37 ± 19; SM: 126 ± 41, P = 0.047) and AA1 positive cells (P: 38 ± 6, SM: 65 ± 17, P = 0.006) were significantly higher after SM than P treatment. The numbers of CD4 (P: 11 ± 10; SM: 32 ± 7, P = 0.085), HLA-DR (P: 65 ± 30; SM: 116 ± 36, P = 0.079) and EG2 positive cells (P: 25 ± 15; SM: 38 ± 26, P = 0.09) tended to increase with SM treatment. In summary, compared to placebo, 1 week of regular use of SM is associated with an increase in bronchial inflammatory cells 24 h after AC. This is in keeping with the recommendation that salmeterol should only be used with an anti-inflammatory agent, particularly in the context of significant allergen exposure. [ABSTRACT FROM AUTHOR]