Capsaicin-sensitive C-fiber-mediated protective responses in ozone inhalation in rats

To assess the role of lung sensory C fibers during and after inhalation of 1 part/million ozone for 8 h, we compared breathing pattern responses and e pithelial injury-inflammation-repair in rats depleted of C fibers by system ic administration of capsaicin as neonates and in vehicle-treated control a nimals. Capsaicin-treated rats did not develop ozone-induced rapid, shallow breathing. Capsaicin-treated rats showed more severe necrosis in the nasal cavity and greater inflammation throughout the respiratory tract than did control rats exposed to ozone. Incorporation of 5-bromo-2'-deoxyuridine (a marker of DNA synthesis associated with proliferation) into terminal bronch iolar epithelial cells was not significantly affected by capsaicin treatmen t; in rats exposed to ozone. However, when normalized to the degree of epit helial necrosis present in each rat studied, there was less 5-bromo-2'-deox yuridine labeling in the terminal bronehioles of capsaicin-treated rats. Th ese observations suggest that the ozone-induced release of neuropeptides do es not measurably contribute to airway inflammation but may play a role in modulating basal and reparative airway epithelial cell proliferation.