You are here:
COMPARISON OF SUSCEPTIBILITY TO INFLUENZA INFECTION IN NASAL EPITHELIAL CELLS OBTAINED FROM SMOKERS AND NON-SMOKERS
Citation:
BRIGHTON, L., J. CARSON, M. A. BECK, AND W. ZHANG. COMPARISON OF SUSCEPTIBILITY TO INFLUENZA INFECTION IN NASAL EPITHELIAL CELLS OBTAINED FROM SMOKERS AND NON-SMOKERS. Presented at American Thoracic Society Annual Meeting, San Diego, CA, May 19 - 24, 2006.
Description:
Several studies have demonstrated that individuals who smoke have greater susceptibility to influenza infections, as well as other respiratory virus infections, than non-smokers, yet the role of airway epithelial cells in this response is not clear. To determine whether in vivo tobacco smoke exposure modifies the susceptibility of airway epithelial cells to influenza, we determined whether cytotoxicity and IL-6 production induced by influenza infections ex vivo is enhanced in nasal epithelial cells obtained from active smokers and if so whether this correlates with urine cotinine levels. Briefly, nasal epithelial cells obtained from non-smokers and active smokers were cultured and differentiated in vitro and infected with influenza. Twenty-four hours post-infection LDH and IL-6 levels in cell culture supernatants were determined to assess the level of cytotoxicity and inflammatory mediator production, respectively. Our results indicate that nasal epithelial cells obtained from smokers were more susceptible to influenza-induced cytotoxicity and IL-6 production as compared to nasal epithelial cells obtained from non-smokers. In addition, the levels of cytotoxicity and IL-6 release were significantly associated with urine cotinine levels, suggesting a relationship between the level of in vivo cigarette smoke exposure and influenza-induced epithelial cell injury ex vivo. Influenza hemagglutin (HA) RNA levels as a marker for viral replication were not elevated in nasal epithelial cells from smokers, suggesting that the effects of smoking status on influenza-induced cytoxicity and IL-6 production was not caused by a greater viral titer. These data suggest that nasal epithelial cells from smokers are more susceptible to influenza-induced epithelial cell injury and that differentiated nasal epithelial cells obtained from smokers could offer a possible in vitro model to study the effects of smoking on influenza infections.