Aims: Tachykinins regulate various biological responses, some of which are potentially relevant in the pathogenesis of chronic obstructive pulmonary disease (COPD). In the lung, tachykinins produce their biological effects by stimulating two specific receptors, neurokinin-1 and -2 receptors (NK-1R and NK-2R). The aim of this study was to quantify NK-1R and NK-2R protein expression in the peripheral lung of smokers with COPD, smokers with normal lung function, and non-smokers. Methods and results: Surgical specimens of 28 smokers (10 with COPD and 18 with normal lung function) and of 9 non-smokers were obtained. Receptor expression was evaluated by immunohistochemical and microscopic analysis. NK-1R and NK2-R were found in alveolar macrophages, pulmonary blood vessels, bronchiolar smooth muscle and bronchiolar blood vessels. NK-2R was also expressed by bronchiolar epithelial cells. Smokers with COPD had a greater percentage of NK-2R+ve alveolar macrophages as compared to smokers with normal lung function and non-smokers. NK-1R and NK-2R expressions were similar in bronchiolar epithelial cells, smooth muscle and blood vessels in the three groups. Conclusions: NK-2R expression was increased in alveolar macrophages of smokers with COPD and may contribute to the amplification of the pulmonary inflammatory response to cigarette smoke in chronic obstructive pulmonary disease
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