Tobacco smoke and airway remodeling in asthma
Abstracts
Initial Award Abstract |
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Several epidemiologic studies of the allergic response in children have implicated environmental tobacco smoke in the exacerbation of allergic disease and asthma. The Environmental Protection Administration estimates that exposure to environmental tobacco smoke exacerbates asthma in up to a million children. Exposure to environmental tobacco smoke has been linked to several adverse asthma outcomes including increased prevalence of asthma, increased severity of asthma symptoms, increased frequency of asthma medication use, and increased emergency room visits by asthmatic children. Asthma studies in mouse models of allergen induced asthma have demonstrated that the combination of environmental tobacco smoke exposure and inhaled allergen results in a significantly enhanced allergic airway immune response (increased levels of airway allergy cells termed eosinophils, increased levels of allergic or IgE antibodies) compared to allergen or tobacco smoke alone. It is currently not known whether environmental tobacco smoke exposure enhances airway remodeling associated with allergen induced asthma and consequently induces irreversible airway hyperreactivity associated with asthma. Thus, the overall hypothesis that we will investigate in a mouse model of asthma is whether the combination of chronic environmental tobacco smoke exposure and allergen, induce remodeling of the airways with resultant sustained and irreversible airway hyperreactivity even in the absence of further environmental tobacco smoke exposure. If this hypothesis were confirmed it would suggest that transient environmental tobacco smoke exposure for example in childhood in an allergic individual could lead to sustained and irreversible asthma as an adult, even if environmental smoke exposure was discontinued. We will also test whether a novel therapy, CpG, can prevent and/or reverse the structural and functional changes induced by exposure to environmental tobacco smoke. |
