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Background: The tachykinins, substance P and neurokinin A, present in sensory nerves and inflammatory cells such as macrophages and dendritic cells, are considered as pro-inflammatory agents. Inflammation of the airways and lung parenchyma plays a major role in the pathogenesis of chronic obstructive pulmonary disease (COPD) and increased tachykinin levels are recovered from the airways of COPD patients. The aim of our study was to clarify the involvement of the tachykinin NK 1 receptor, the preferential receptor for substance P, in cigarette smoke (CS)-induced pulmonary inflammation and emphysema in a mouse model of COPD.

The tachykinins substance P and neurokinin A are found within airway nerves and immune cells. They have various effects on the airways that can contribute to the changes observed in asthma and chronic obstructive pulmonary disease. Both tachykinin NK(1) and NK(2) receptors have been involved in the bronchoconstriction and the proinflammatory changes induced by substance P and neurokinin A. Tachykinin NK(1) and NK(2) receptor antagonists have activity in various animal models of allergic asthma and chronic bronchitis. It is suggested that dual NK(1)/NK(2) and triple NK(1)/NK(2)/NK(3) tachykinin receptor antagonists have potential in the treatment of obstructive airway diseases.

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