Effect of ozone on susceptibility to respiratory viral infection and virus-induced cytokine secretion.

Airway epithelium is the primary target tissue for respiratory viruses as well as an important target of ozone (O(3)) toxicity. A change in the severity of viral airway infection may result from changes in epithelial cell susceptibility to infection, metabolic interference with viral replication, or altered production of immune regulatory molecules by the infected cells as a result of exposure to O(3). In this study we have investigated whether O(3) exposure alters the susceptibility of human airway epithelial cells to respiratory syncytial virus (RSV) infection, the production of infectious virus, and/or release of virus-induced cytokines IL-6 and IL-8. The epithelial cell line BEAS-2B grown on collagen-impregnated filters was exposed to O(3) (0.5 ppm for 60 min) or filtered air immediately before or 24 h after infection with RSV. Cells exposed to O(3) before RSV infection released 44% less virus over 4 days of infection while O(3) exposure post RSV infection had no effect on virus production. O(3) exposure preceding RSV infection showed short term additive effects of these treatments on epithelial cell IL-6 and IL-8 production, a decrease in cytokines at 48 h, but did not affect long term cytokine production by RSV-infected cells. Furthermore, O(3) exposure did not affect long term cytokine production by cells with an established RSV infection at the time of exposure. These data suggest that O(3) does not adversely affect viral airway infection, at least not on the level of the host cell for viral replication.