Neutrophils injure bronchial epithelium after ozone exposure

Neutrophil (PMN) influx is an early, prominent finding in the airways of hu mans after experimental inhalation of ozone (O3), however the potential for PMN to contribute to epithelial injury in this setting is unknown. Bronchi al epithelial cells of the human BEAS 2B R1.4 cell line or primary human br onchial epithelial cells underwent DNA labeling by incubation with BrdU. Mo nolayers were exposed to O3 (0.05 to 1 ppm) or filtered air for 60 min., an d subsequently incubated with PMN for 2 h. Epithelial cell cytolysis was si gnificant only in BEAS exposed to O3 and co-cultured with PMN. Apoptosis wa s maximal in BEAS exposed to O3 + PMN. Primary bronchial epithelial cells w ere resistant to injury; no cytolysis was detected, and apoptosis was detec ted only after treatment with 10 mM H2O2. Neutrophils may increase damage t o the respiratory epithelium after O3 exposure, but primary bronchial epith elial cells are resistant to PMN and ozone induced injury.