Expression of the beta 6 integrin subunit is associated with sites of neutrophil influx in lung epithelium

Inhalation of ozone by Rhesus monkeys results in epithelial injury and gran ulocyte influx in both conducting airways and respiratory bronchioles. We h ave reported that ozone-induced neutrophil recruitment and subsequent epith elial repair can be inhibited in vivo with a CD18 antibody. The antibody-me diated effect is abrogated by local instillation of C5a (a CD18-independent neutrophil chemoattractant), thereby demonstrating a role for neutrophils in lung epithelial repair processes. As an extension of this study, we exam ined the effect of ozone and neutrophil influx on epithelial expression of the beta6 integrin, an adhesion molecule associated with proliferation and repair. Expression of beta6 integrin was determined by immunohistochemistry for ozone-exposed monkeys treated with either control immunoglobulins or a CD18 antibody. The tracheal epithelium of ozone-exposed monkeys treated wi th control immunglobulins expressed the beta6 integrin. In contrast, the tr acheal epithelium of ozone-exposed monkeys treated with CD18 antibody exhib ited very low to undetectable expression of beta6 integrin. In association with C5a instillation and neutrophil influx, beta6 integrin was also observ ed in respiratory bronchiolar epithelium from both control and ozone-expose d animals. These findings cumulatively suggest that lung epithelial cell ex pression of beta6 integrin is associated with sites of neutrophil recruitme nt.