Effects of chronic cigarette smoke exposure on lung inflammation in ovalbumin-sensitized mice

Introduction: Several studies have identified smoking as a risk factor for development of asthma, but others have failed to find such an association. Objective: To compare the effects of long cigarette smoke exposure once or twice a day in a model of chronic allergic pulmonary inflammation. Methods: Balb/c mice were sensitized with ovalbumin (OVA) and alum and challenged with an aerosol of OVA. The cigarette smoke groups were exposed to cigarette smoke once or twice a day for thirty consecutive days. Control groups (SAL) received alum only. Twenty-four hours after the last challenge, we evaluated the lung responsiveness, lung inflammation and the production of cytokines and OVA-specific antibodies (IgG1, IgG2a and IgE). Results: OVA-sensitized mice showed increased responsiveness, lung eosinophilia and elevated production of cytokines (IL-4, -5, -10, TSLP) in lung as well as great production IgG1, IgG2a and IgE anti-OVA. The co-exposure of sensitized mice to chronic cigarette smoke once a day decreased the numbers of eosinophils and neutrophils in airways and increased IL-10, IL-13 and TSLP. While twice a day of co-exposure to cigarette smoke decreased IgE production and eosinophil influx in airway. However, these mice showed an increase in the production of IL-10. Comparing both protocols of co-exposition, OVA group co-exposed twice a day to cigarette smoke showed a decreased of IL-13, TSLP, IL-10 when compared to OVA group co-exposed only once a day. Conclusion: Co-exposition of chronic cigarette smoke once and twice a day regulates lung inflammation by increasing regulatory cytokine IL-10 while twice a day also decreased IgE level.