To investigate the relationship between neutrophils and the repair of epithelium in specific airway generations of the tracheobronchial tree following short-term )3 exposure, we exposed rhesus monkeys for 8 hours to 0.00 (controls) or 0.8 ppm O3, followed by 24 or 48 hours in filtered air before necropsyt. Two groups of monkeys were given anti-CD18 monoclonal antibodies (Ab) by the cephalic vein at 2 mg/kg BW, 16 hours prior to exposure and every 24 hours thereafter. There were six control monkeys and four monkeys in each of two groups at 24 or 48 hours with and without anti-CD18 antibody. At necropsy the right caudal lung lobe was lavaged, the right middle lung lobe was fixed by instillation and the left caudal lung lobe was fixed by vascular perfusion. Lavage neutrophils were significantly elevated in normal monkeys exposed to O3 as compared with other groups. Ab-treated O3 monkeys at 24 hours showed an 18 fold inhibition of neutrophils in lavage as compared with normal O3 monkeys at 24 hours. Repair of respiratory bronchiolar epithelium was markedly delayed at 24 and 48 hours in Ab-treated O3 monkeys as compared with normal O3 monkeys. The respiratory bronchiolar epithelium showed hypertrophied nonciliated bronchiolar cells, abundant airway inflammatory cells (neutrophils and alveolar macrophages) and few degenerative epithelial cells in normal O3 monkeys 24 hours after exposure. In contrast, respiratory bronchioles of Ab-treated O3 monkeys showed marked epithelial soughing and necrosis and fewer airway inflammatory cells at 24 hours after exposure. Neutrophils were observed in capillaries of respiratory bronchioles next to injured epithelium and bare epithelial basal lamina in Ab-treated O3 monkeys, but only an occasional neutrophil was observed in airway lumina. We interpret these results as evidence for the contribution of neutrophils to the repair of the respiratory bronchiole epithelium after short-term O3 inhalation.
Showing the most recent 10 out of 408 publications
