Cigarette Smoke Differentially Affects Eosinophilia and Remodeling in a Model of House Dust Mite Asthma

Abstract

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.

Short cigarette smoke exposure facilitates sensitisation and asthma development in mice

“…Although different in experimental setup, they found some indications for increased allergic inflammation due to cigarette smoke; however, these were less pronounced than in our model. In contrast to our current findings, a recent study by BOTELHO et al [37] using a murine model of established allergic asthma, reported significantly attenuated eosinophilia in BAL fluid of mice exposed to both HDM and cigarette smoke, together with decreased mucus production, and no difference in CD4 + T-cell activation nor airway hyperresponsiveness between HDM and, or cigarette smokeexposed mice.…”

“…In addition, the variability between commercially available preparations of HDM extract (e.g. endotoxin content) may affect the development of potential Th2 responses in the lung [37].…”

The Long-term Clinical Course of Chronic Eosinophilic Pneumonia

“…To our knowledge, no other reports have assessed the predictive factors of CEP relapse. One possible explanation of our results is the contribution of smoking to the development or maintenance of eosinophilic infiltration in the lung (16). Although our understanding of the pathophysiology of CEP is incomplete, studies of BAL fluid from patients with CEP show elevations of several cytokine, chemokine, and immunomodulatory products (17)(18)(19), which suggests that a multifactorial process is involved in the recruitment of eosinophils into the lung (20).…”

Clinical Variants of Allergic Rhinitis and Asthma Phenotypes in Patients with or Without a Smoking History

“…(8.62%5.14 vs.15.22%4.97, p<0.01) ( Table 14). As it is known that smokers have higher levels of total immunoglobulin E (IgE) 48 and a greater degree of infiltration of inflammatory cells, especially eosinophils 49 , in comparison to nonsmokers, it is most likely that inflammatory processes will lead to airways remodeling and fixed bronchial obstruction, with lower reversibility. As far as skin sensitization established on the basis of skin prick tests is concerned, a greater number of patients from the smoking group (active and former smokers) were sensitized to perennial allergens, while the non-smoking patients with allergic asthma and rhinitis were more sensitized to seasonal allergens.…”