Neuropeptide-induced chemotaxis of eosinophils in pulmonary diseases.

Eosinophilic lung diseases include various disease entities, and the incidence of pulmonary infiltration with eosinophilia is on the rise. Because eosinophils, well known as inflammatory cells, respond to peripheral neuropeptides in vitro and in vivo, and these peptides are also present in human airway nerves, their interactions are thought to play a major role in the initiation and perpetuation of inflammatory lung diseases. This article reviews the current literature on eosinophil biology and interactions of these cells with the neuroendocrine system. Also, implications of tachykinins and other neuropeptides in eosinophilic pulmonary diseases is discussed based on recently investigated mechanisms. Eosinophils and sensory nerves most likely influence each other in a two-directional way in the pathogenesis of pulmonary diseases. Although release of sensory neuropeptides is involved in most conditions of airway hyperresponsiveness, increased bronchial resistance, and lung eosinophilia, the role of these nervous system-derived mediators in pulmonary diseases may be underestimated.