Immunomodulatory role of acute cigarette smoke exposure in pdmH1N1 and H9N2 infection (170.14)

Abstract Cigarette smoke has both immune-activating and suppressing activities. Mouse studies have demonstrated that smoke exposure increases the expressions of some factors likely to be important in the antiviral defense. However, there is no report about the role of cigarette smoke in 2009 pandemic H1N1 (pdmH1N1) and avian influenza A H9N2 (H9N2/G1) infection. In this study, C57/B6N mice were whole body exposed to 4% cigarette smoke 4 hours per day for 21 days and then infected with pdmH1N1 or H9N2 virus. Some mice were exposed to room air in parallel as the control group. Mortality, weight changes, lung virus loads and inflammatory cytokines and chemokines were analyzed. For pdmH1N1 infection, although no significant difference in the lung virus loads was shown between the two groups, smoke exposure group had a significantly lower mortality than the air exposure group, which may be caused by the lower inflammatory response in the smoke exposure group than in the air exposure group at day 5 post virus infection. Similarly, after H9N2 virus infection, the mice in smoke exposure group displayed a significantly milder disease, as evidenced by a less weight loss, as well as lower inflammatory response compared to the air exposure group. Our study provided the first in vivo evidence that acute cigarette smoke exposure may modulate the effect of influenza A virus infection. The underlying mechanism is under investigation.