US EPA, National Health and Environmental Effects Research Laboratory, Human Studies Division, , Research Triangle Park, NC 27711, USA.
Environ Toxicol Pharmacol. 1998 Dec 1;6(4):257-65. doi: 10.1016/s1382-6689(98)00043-x.
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.
气道上皮细胞是呼吸道病毒的主要靶组织，也是臭氧（O3）毒性的重要靶组织。病毒呼吸道感染严重程度的变化可能是由于上皮细胞对感染的敏感性变化、病毒复制的代谢干扰，或由于暴露于 O3，感染细胞产生免疫调节分子的改变所致。在这项研究中，我们研究了 O3 暴露是否改变了人呼吸道上皮细胞对呼吸道合胞病毒（RSV）感染的易感性、传染性病毒的产生和/或病毒诱导的细胞因子 IL-6 和 IL-8 的释放。在胶原浸渍滤器上生长的上皮细胞系 BEAS-2B 在 RSV 感染前或感染后 24 小时用 O3（0.5ppm 60 分钟）或过滤空气暴露。在 RSV 感染前暴露于 O3 的细胞在感染后 4 天的病毒释放量减少了 44%，而 O3 暴露后感染 RSV 对病毒产生没有影响。在 RSV 感染前暴露于 O3 显示出这些处理对上皮细胞 IL-6 和 IL-8 产生的短期附加效应，在 48 小时时细胞因子减少，但不影响 RSV 感染细胞的长期细胞因子产生。此外，O3 暴露在暴露时对已经建立的 RSV 感染细胞的长期细胞因子产生没有影响。这些数据表明，O3 对病毒呼吸道感染没有不利影响，至少对病毒复制的宿主细胞没有不利影响。
