Neutrophil oxygen metabolite inhibition of cultured chinchilla middle ear epithelial cell growth.

Middle ear inflammation in acute bacterial otitis media is characterized by accumulation of neutrophils in middle ear effusion. Since neutrophils release products that may injure surrounding tissues, we studied the effect of neutrophil metabolic products on middle ear epithelial cells (MEECs) in vitro. Chinchilla MEECs were incubated with phorbol myristate acetate (PMA)-activated human neutrophils or with hydrogen peroxide (H2O2). Cell growth, which was measured by 3H-thymidine incorporation, was inhibited by activated neutrophils and by H2O2. Unstimulated neutrophils, PMA alone, and catalase alone did not affect the viability of MEECs. Catalase, an enzyme that reduces H2O2, partially blocked the inhibitory effect of activated neutrophils and completely blocked the inhibitory effect of H2O2. Inhibition of MEEC metabolism by neutrophil-reactive oxygen species may contribute to epithelial injury, which may prolong the middle ear inflammatory response and lead to chronic tissue damage.