Cigarette smoking in asthmatics is known to cause severe symptoms, pulmonary dysfunction, neutrophilic inflammation, and decreased glucocorticoid sensitivity. The differential effects of dexamethasone (Dex) and roflumilast (Rof) on airway inflammation, lung function and airway responsiveness in ovalbumin-induced asthmatic mice with or without concurrent cigarette smoke (CS) exposure were examined.
　In the CS-exposed asthmatic mice, the airway neutrophils and lung compliance were increased, and the central airways resistance (Rn) and airway hyperreactivity (AHR) were decreased when compared with the asthmatic mice. Dex inhibited the airway eosinophils, airway resistance (Raw) and AHR in the asthmatic mice. In the CS-exposed asthmatic mice, Dex reduced the airway eosinophils but exacerbated the airway neutrophils, lung tissue resistance and AHR. Rof decreased the Rn in the asthmatic mice, but did not affect in the CS-exposed asthmatic mice.
　Based on these results, in asthmatic mice with CS exposure, Dex was effective in reducing eosinophilic inflammation but exacerbated the neutrophilic inflammation, lung tissue resistance and AHR. Rof was ineffective in improving inflammation and lung function in asthmatic mice with CS exposure.