![Sample our Medicine, Dentistry, Nursing & Allied Health journals, sign in here to start your FREE access for 14 days]({"type":"image" , "src" : "/sda/5944/TOC-Subject-Sample-2021-Medicine-Dentistry-Nursing-Allied-Health.jpg"})
Abstract
The aims of the present study were to determine whether β2-agonists (short-and long-acting) and a glucocorticoid (budesonide) influence the secretion of a pro-inflammatory cytokine (interleukin-1, [IL-1]) and a granulocyte attractant (leukotriene B4 [LTB4]) and to compare these effects on blood monocyte and alveolar macrophages.
Alveolar macrophages (obtained by bronchoalveolar lavage) and blood monocytes from 26 healthy nonsmokers were stimulated with lipopolysaccharide or human serum opsonized zymosan. The influence of four β2-agonists (salbutamol, terbutaline, formoterol, and salmeterol) and a corticosteroid (budesonide) on the release of interleukin-1β (IL-1β) and LTB4 was studied in a dose-response manner (10-−8-10-−5 mol/L for β2-agonists and 10-−10-10-−6mol/L for budesonide).
The stimulated IL-1β secretion was significantly greater in blood monocytes than in alveolar macrophages (p < 0.05), but alveolar macrophages were much more capable of secreting LTB4 than were blood monocytes (p < 0.001). Budesonide significantly inhibited the release of IL-1β from blood monocytes (p < 0.001), but no such effect was observed in alveolar macrophages. Budesonide did not influence the release of LTB4 in either cell type. The β2-agonists neither influenced the LTB4 nor the IL-β secretion in either cell type with the exception of formoterol, which stimulated IL-1β secretion at the highest concentration (10-−5mol/L, p < 0.05).
In conclusion, β2-agonists exhibited only minor effects on IL-1β secretion from blood monocytes and no effect on LTB4-secretion from either cell type, and budesonide effectively inhibited the IL-1β release in blood monocytes, but not in alveolar macrophages. Thus, induced secretion of LTB4 and IL-1β, and the sensitivity to corticosteroids with regard to IL-1β secretion, change during the transformation from blood monocytes to alveolar macrophages.