Inhalation of ozone by Rhesus monkeys results in epithelial injury and granulocyte influx in both conducting airways and respiratory bronchioles. We have reported that ozone-induced neutrophil recruitment and subsequent epithelial repair can be inhibited in vivo with a CD18 antibody. The antibody-mediated 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 examined the effect of ozone and neutrophil influx on epithelial expression of the β6 integrin, an adhesion molecule associated with proliferation and repair. Expression of β6 integrin was determined by immunohistochemistry for ozone-exposed monkeys treated with either control immunoglobulins or a CD18 antibody. The tracheal epithelium of ozoneexposed monkeys treated with control immunglobulins expressed the β6 integrin. In contrast, the tracheal epithelium of ozone-exposed monkeys treated with CD18 antibody exhibited very low to undetectable expression of β6 integrin. In association with C5a instillation and neutrophil influx, β6 integrin was also observed in respiratory bronchiolar epithelium from both control and ozone-exposed animals. These findings cumulatively suggest that lung epithelial cell expression of β6 integrin is associated with sites of neutrophil recruitment.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Histochemistry and Cytochemistry|
|State||Published - 2001|
ASJC Scopus subject areas
- Cell Biology