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Background：Asthmatic airway inflammation is mediated by allergen-specific Th2response. Activation of PPARy is found to inhibit the airway inflammation in asthmatic models.however, the mechanism(s) underlying the action of PPARy activation in allergic airwayinflammation has not been revealed clearly. Methods：To investigate the role of PPARyactivation in allergic airway inflammation and to determine whether PPARy activation couldmodulate the balance of Th1/Th2 response, we examined the effects of PPARy activation onallergic airway inflammation, the levels of GATA-3 and T-bet mRNA transcripts in a murineasthmatic model. Results：Our data showed that treatment with Rosiglitazone significantlyreduced eosinophilia and mucous overproduction in the lungs. Furthermore, PPARy activationsignificantly down-regulated the levels of GATA-3 mRNA transcript, but increased theexpression of T-bet.Conclusions：Our data suggest that PPARy activation inhibits allergicairway inflammation in asthmatic mice by down-regulating allergen-induced predominate Th2responses, but enhancing Thl response, modulating the balance of Th2/Th1 responses.