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Departments of 1 Anatomy,
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 epithelial
injury-inflammation-repair in rats depleted of C fibers by systemic
administration of capsaicin as neonates and in vehicle-treated control
animals. 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 bronchiolar epithelial cells was not
significantly affected by capsaicin treatment in rats exposed to ozone.
However, when normalized to the degree of epithelial necrosis present
in each rat studied, there was less 5-bromo-2'-deoxyuridine labeling in the terminal bronchioles of capsaicin-treated rats. These observations suggest that the ozone-induced release of neuropeptides does not measurably contribute to airway inflammation but may play a role in
modulating basal and reparative airway epithelial cell proliferation.
C fibers; ozone; 5-bromo-2'-deoxyuridine labeling; morphometry; rapid, shallow breathing
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