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IL-18 Gene Transfer by Adenovirus Prevents the Development of and Reverses Established Allergen-Induced Airway Hyperreactivity¹

David M. Walter^*, Carmen P. Wong, Rosemarie H. DeKruyff^*, Gerald J. Berry, Shoshana Levy and Dale T. Umetsu^2,*

^* Division of Immunology and Allergy, Department of Pediatrics, Division of Oncology, Department of Medicine, and Department of Pathology, Stanford University Medical Center, Stanford, CA 94305

We examined the role of IL-18 in preventing the development of and in reversing established allergen-induced airway inflammation and airway hyperreactivity (AHR), the cardinal features of asthma. IL-18, which potently induces IFN-, was administered into the respiratory tract as cDNA in a replication-deficient adenovirus (Adv). Treatment of OVA-sensitized mice with the IL-18-expressing Adv reduced allergen-specific IL-4 production, airway eosinophilia, and mucus production, increased IFN- production, and prevented the development of AHR. The effects of the IL-18 Adv treatment were dependent on the presence of IFN- and IL-12. Moreover, administration of the IL-18 Adv to mice with established AHR greatly reduced AHR and IL-4 production and increased IFN- production. These results demonstrate that IL-18, when administered by Adv into the respiratory tract, effectively reduces AHR and replaces an established Th2-biased immune response with a Th1-biased response.

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