Exposure to cigarette smoke downregulates β2-adrenergic receptor expression and upregulates inflammation in alveolar macrophages

Cigarette smoke-triggered inflammation is important in the pathophysiology of chronic obstructive pulmonary disease (COPD). beta(2)-Adrenergic receptor (beta(2)-AR) is abundantly expressed on inflammatory cells, which is associated with inflammation regulation. To observe alterations in inflammation, pathological changes in lung tissues, and detect changes in beta(2)-AR expression, rats were exposed for 4 months to cigarette smoke. Pathological changes were observed in lung tissue sections. The levels of inflammatory mediators tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta in bronchoalveolar lavage fluid (BALF), and lung tissues were measured using enzyme-linked immunosorbent assay (ELISA). Nuclear factor (NF)-kappa B activity was detected by electrophoretic mobility shift assay (EMSA). Exposure to this regimen of cigarette smoke induced peribronchial and perivascular lymphocytic aggregates and parenchymal accumulation of macrophages in rats. EMSA demonstrated that smoke exposure enhanced NF-kappa B activation in rats' alveolar macrophages (AMs). Compared with the control group, smoke exposure induced a notable increase in TNF-alpha and IL-1 beta in BALF, lung tissues, and a decrease of beta(2)-AR expression of AMs. The expression of beta(2)-AR from AMs was inversely correlated with TNF-alpha and IL-1 beta levels of BALF. These data demonstrated that chronic smoke-triggered lung inflammation was accompanied by down-regulation of beta(2)-AR in rat lungs' AMs.