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Coexposure to Environmental Tobacco Smoke Increases Levels of Allergen-Induced Airway Remodeling in Mice¹

Myung Goo Min^2,*, Dae Jin Song^2,*,, Marina Miller^*, Jae Youn Cho^*, Shauna McElwain^*, Paul Ferguson^* and David H. Broide^3,*

^* Department of Medicine, University of California-San Diego, La Jolla, CA 92093; and Department of Pediatrics, College of Medicine, Korea University, Seoul, Korea

Environmental tobacco smoke (ETS) can increase asthma symptoms and the frequency of asthma attacks. However, the contribution of ETS to airway remodeling in asthma is at present unknown. In this study, we have used a mouse model of allergen-induced airway remodeling to determine whether the combination of chronic exposure to ETS and chronic exposure to OVA allergen induces greater levels of airway remodeling than exposure to either chronic ETS or chronic OVA allergen alone. Mice exposed to chronic ETS alone did not develop significant eosinophilic airway inflammation, airway remodeling, or increased airway hyperreactivity to methacholine. In contrast, 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. Mice coexposed to chronic ETS and chronic OVA allergen had significantly increased levels of eotaxin-1 expression in airway epithelium which was associated with increased numbers of peribronchial eosinophils, as well as increased numbers of peribronchial cells expressing TGF-1. These studies suggest that chronic coexposure to ETS significantly increases levels of allergen-induced airway remodeling (in particular smooth muscle thickness) and airway responsiveness by up-regulating expression of chemokines such as eotaxin-1 in airway epithelium with resultant recruitment of cells expressing TGF-1 to the airway and enhanced airway remodeling.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Tobacco-Related Disease Research Program Grant 12RT-0071 (to D.H.B.).

² M.G.M. and D.J.S. contributed equally as first authors to this manuscript.

³ Address correspondence and reprint requests to Dr. David H. Broide, University of California-San Diego, Basic Science Building, Room 5090, 9500 Gilman Drive, La Jolla, CA 92093-0635. E-mail address: dbroide{at}ucsd.edu

⁴ Abbreviations used in this paper: ETS, environmental tobacco smoke; AHR, airway hyperreactivity; Mch, methacholine; BAL, bronchoalveolar lavage; MBP, major basic protein; CTGF, connective tissue growth factor; PAS, periodic acid-Schiff.

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