title: Environmental tobacco smoke exposure does not prevent corticosteroids reducing inflammation, remodeling, and airway hyperreactivity in mice exposed to allergen.
abstract: The ability of corticosteroids to reduce airway inflammation and improve lung function is significantly reduced in asthmatics who are tobacco smokers compared with asthmatics who are nonsmokers. As not only high levels of tobacco smoke exposure in active smokers, but also significantly lower levels of tobacco smoke exposure from passive environmental tobacco smoke (ETS) exposure in nonsmokers can increase both asthma symptoms and the frequency of asthma exacerbations, we utilized a mouse model to determine whether corticosteroids can reduce levels of airway inflammation, airway remodeling, and airway hyperreactivity in mice exposed to the combination of chronic ETS and ovalbumin (OVA) allergen. Chronic ETS exposure alone did not induce increases in eosinophilic airway inflammation, airway remodeling, or airway hyperreactivity. Mice exposed to chronic OVA allergen had significantly increased levels of peribronchial fibrosis, increased thickening of the smooth muscle layer, increased mucus, and increased airway hyperreactivity, which was significantly enhanced by coexposure to the combination of chronic ETS and chronic OVA allergen. Administration of corticosteroids to mice exposed to chronic ETS and OVA allergen significantly reduced levels of eosinophilic airway inflammation, mucus production, peribronchial smooth muscle thickness, airway hyperreactivity, and the number of peribronchial TGF-beta1+ cells. Overall, this study demonstrates that corticosteroids can significantly reduce levels of eosinophilic inflammation, mucus expression, airway remodeling, and airway hyperreactivity in chronic ETS-exposed mice challenged with allergen.
authors.affiliation: Department of Medicine, University of California San Diego, 92093-0635, USA.
authors.forename: Dae Jin
authors.initials: DJ
authors.lastname: Song
authors.forename: Myung Goo
authors.initials: MG
authors.lastname: Min
authors.forename: Marina
authors.initials: M
authors.lastname: Miller
authors.forename: Jae Youn
authors.initials: JY
authors.lastname: Cho
authors.forename: David H
authors.initials: DH
authors.lastname: Broide
mesh_terms: D000305:Adrenal Cortex Hormones / Q000494:pharmacology*; D000485:Allergens / Q000276:immunology / Q000494:pharmacology; D000818:Animals; D001249:Asthma / Q000188:drug therapy / Q000209:etiology / Q000276:immunology; D001980:Bronchi / Q000276:immunology / Q000473:pathology; D016535:Bronchial Hyperreactivity / Q000188:drug therapy / Q000209:etiology / Q000276:immunology; D004195:Disease Models, Animal; D004804:Eosinophils / Q000276:immunology; D005260:Female; D005355:Fibrosis; D051379:Mice; D008807:Mice, Inbred BALB C; D009093:Mucus / Q000187:drug effects / Q000276:immunology; D009130:Muscle, Smooth / Q000276:immunology / Q000473:pathology; D010047:Ovalbumin / Q000276:immunology / Q000494:pharmacology; D011014:Pneumonia / Q000188:drug therapy / Q000209:etiology / Q000276:immunology; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*; D053773:Transforming Growth Factor beta1 / Q000276:immunology / Q000378:metabolism
chemical_list: D000305:Adrenal Cortex Hormones; D000485:Allergens; D014028:Tobacco Smoke Pollution; D053773:Transforming Growth Factor beta1; D010047:Ovalbumin