Abstract
Introduction: Asthmatics smokers have an accelerated decline in lung function compared with non-smokers. However, some clinical trials suggest that smokers have a lower risk of developing asthma symptoms when compared with nonsmokers and ex-smokers. Objective: To compare the effects of twelve or thirty days of exposition to cigarette smoke in a model of chronic allergic pulmonary inflammation. Methods: Balb/c mice were sensitized and challenged with ovalbumin (OVA) following two different experimental protocols: a short (28 days) or a long protocol (50 days). Mice were co-exposed to cigarette smoke daily for twelve (short protocol) or thirty days (long protocol). 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: Longer protocol of sensitization showed an increase in lung responsiveness as well as in the levels of IL-4 and OVA-specific antibodies. While, the shorter protocol lead to an increase in the production of IL-5, IL-13, IL-10 as well as TGF-β and OVA-specific antibodies. The co-exposition of sensitized mice to cigarette smoke for thirty days increased the IL-10 level and reduced the lung responsiveness although increased IL-13 production. Additionally, after twelve days of co-exposition to cigarette smoke, sensitized mice increased IL-10 production and decreased IgG2a level. Conclusion: Co-exposition of cigarette smoke for twelve days worse lung inflammation by decreasing humoral regulation while thirty days of co-exposition increased cellular response although reverting lung hyperresponsiveness.
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