Cigarette Smoke Differentially Affects Eosinophilia and Remodeling in a Model of House Dust Mite Asthma
Department of Pathology and Molecular Medicine, Centre for Gene Therapeutics, McMaster University, 1200 Main Street West, Hamilton, ON, L8N 3Z5 Canada.American Journal of Respiratory Cell and Molecular Biology (Impact Factor: 3.99). 02/2011; 45(4):753-60. DOI: 10.1165/rcmb.2010-0404OC
Although a similar prevalence of smoking is evident among patients with asthma and the general population, little is known about the impact of cigarette smoke on the immune inflammatory processes elicited by common environmental allergens. We investigated the impact of exposure to cigarette smoke on house dust mite (HDM)-induced allergic airway inflammation and its consequences for tissue remodeling and lung physiology in mice. BALB/c mice received intranasal HDMs daily, 5 days per week, for 3 weeks to establish chronic airway inflammation. Subsequently, mice were concurrently exposed to HDMs plus cigarette smoke, 5 days per week, for 2 weeks (HDMs + smoke). We observed significantly attenuated eosinophilia in the bronchoalveolar lavage of mice exposed to HDMs + smoke, compared with animals exposed only to HDMs. A similar activation of CD4 T cells and expression of IL-5, IL-13, and transforming growth factor-β was observed between HDM-treated and HDM + smoke-treated animals. Consistent with an effect on eosinophil trafficking, HDMs + smoke exposure attenuated the HDM-induced expression of eotaxin-1 and vascular cell adhesion molecule-1, whereas the survival of eosinophils and the numbers of blood eosinophils were not affected. Exposure to cigarette smoke also reduced the activation of B cells and the concentrations of serum IgE. Although the production of mucus decreased, collagen deposition significantly increased in animals exposed to HDMs + smoke, compared with animals exposed only to HDMs. Although airway resistance was unaffected, tissue resistance was significantly decreased in mice exposed to HDMs + smoke. Our findings demonstrate that cigarette smoke affects eosinophil migration without affecting airway resistance or modifying Th2 cell adaptive immunity in a murine model of HDM-induced asthma.
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ABSTRACT: Rhinitis is a common disease, and its prevalence is increasing worldwide. Several studies have provided evidence of a strong association between asthma and rhinitis. Although smoking and obesity have been extensively analyzed as risk factors of asthma, associations with rhinitis are less clear. The aims of our study were (i) to evaluate the prevalence of rhinitis using the European Community Respiratory Health Survey (ECRHS) questionnaire in Japanese adults and (ii) to evaluate the associations of smoking and body mass index (BMI) with rhinitis. Following our study conducted in 2006-2007 to determine the prevalence of asthma using the ECRHS questionnaire, our present analysis evaluates the prevalence of rhinitis and its association with smoking and BMI in Japanese adults 20-79 years of age (N = 22819). We classified the subjects (20-44 or 45-79 years) into four groups as having (i) neither rhinitis nor asthma; (ii) rhinitis without asthma; (iii) asthma without rhinitis; or (iv) rhinitis with asthma. We then evaluated associations with smoking and BMI in each group. The overall age-adjusted prevalence of rhinitis was 35.1% in men and 39.3% in women. A higher prevalence was observed in the younger population than in the older population. Active smoking and obesity were positively associated with asthma without rhinitis. In contrast, particularly in the 20- to 44-year age-group, active smoking and obesity were negatively associated with rhinitis without asthma. The results of the present study suggest that smoking and obesity may have different effects on the development of rhinitis and asthma.Allergy 02/2012; 67(5):653-60. DOI:10.1111/j.1398-9995.2012.02793.x · 6.03 Impact Factor
- Allergic Rhinitis, 03/2012; , ISBN: 978-953-51-0288-5
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ABSTRACT: Epidemiological studies indicate that cigarette smoke (CS) exposure is a risk factor for increased sensitization and asthma development. The aim of the study was to examine the impact of CS on sensitization and allergic airway inflammation, in response to a low dose of house dust mite (HDM), and to obtain potential mechanistic insights.Mice were exposed to low doses of HDM extract combined with air or CS exposure, either during allergen sensitization or during development of allergic airway disease.Mice concomitantly exposed to low dose HDM, combined with CS for 3 weeks, demonstrated an asthmatic phenotype with significantly increased airway eosinophilia, goblet cell metaplasia, airway hyperresponsiveness and a rise in HDM-specific serum IgG1, compared to sole HDM or CS exposure. In addition, short CS inhalation, during the initial contact with HDM allergens, was sufficient to facilitate sensitization and development of a complete asthmatic phenotype after rechallenge with HDM. Mechanistically, short CS exposure amplified DC-mediated transport of FITC-labelled HDM allergens to the intrathoracic lymph nodes and generated a local Th2 response.Short CS exposure is sufficient to facilitate allergic sensitization and the development of low dose HDM-induced allergic asthma, possibly through affecting dendritic cell function.European Respiratory Journal 08/2012; 41(5). DOI:10.1183/09031936.00096612 · 7.64 Impact Factor
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