Tiotropium sustains the anti-inflammatory action of olodaterol via the cyclic AMP pathway.

摘要: Mesenchymal cells (fibroblasts) of the airway wall respond to cholinergic stimulation by releasing pro-inflammatory and chemotactic cytokines may thus contribute chronic inflammation lung. Here, we studied anti-inflammatory potential olodaterol, a long acting β2-adrenergic receptor agonist, tiotropium, long-acting muscarinic antagonist, whether they interact at level cyclic AMP dependent signaling pathway. Pulmonary fibroblasts asthmatic (n = 9) non-asthmatic 8) subjects were stimulated with agonist carbachol interleukin-1β (IL-1 beta) in presence or absence tiotropium olodaterol alone, their combination. We also measured cAMP levels phosphorylation response element binding protein (CREB). As single components, carbachol, did not affect IL-6 IL-8 release. Carbachol concentration-dependently enhanced production IL-1β-induced IL-8, which was blocked simultaneous addition tiotropium. The combination plus further reduced Olodaterol induced CREB, an effect counteracted but rescued conclude that cooperate decrease inflammatory pulmonary vitro.