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-beta1. 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-beta1 to the airway and enhanced
airway remodeling.