[Effect of capsaicin on the migration of eosinophils into the bronchi of guinea pigs].

Substance P (SP), a potent neuropeptide, which is localized in the sensory nerves and released by many physiological stimuli has been implicated in airway neurogenic inflammation. We have studied the effects of capsaicin (CAP), which releases tachykinins (TK) from the sensory nerves, on eosinophil (EOS) recruitment in the airway in guinea pigs in vivo. Male guinea pigs were used. The respiratory resistance (Rrs) of the guinea pigs were measured by an oscillation technique and histological studies of the right main bronchus were carried out. Exposure to inhaled CAP resulted in a significant increase in Rrs with PC200 CAP of 0.97 +/- 0.25 (x 10(-6) M) (n = 5). This stimulation also provoked striking eosinophilia in the right bronchus in a dose-dependent manner. A neutral endopeptidase (NEP) inhibitor, phosphoramidon, potentiated CAP-induced EOS infiltration. By contrast, pretreatment with [D-Pro2, D-Trp7,9]-SP, an analogue of SP and its receptor antagonist, diminished the response. We conclude that CAP-induced tachykinin release is capable of causing striking eosinophilia in the lung in vivo. This mechanism may contribute to airway inflammation in patients with asthma. This would provide further support for a link between tachykinin and bronchial eosinophilia in asthma.