Adenoviral gene transfer of the NF-κB inhibitory protein ABIN-1 decreases allergic airway inflammation in a murine asthma model

Airway inflammation is a characteristic of many lung disorders, including asthma and chronic obstructive pulmonary disease. Using a murine model of allergen-induced asthma, we have demonstrated that adenovirus-mediated delivery of the nuclear factor-kappa B (NF-kappa B) inhibitory protein ABIN-1 to the lung epithelium results in a considerable reduction of allergen-induced eosinophil infiltration into the lungs. This is associated with an ABIN-1-induced decrease in allergen-specific immunoglobulin E levels in serum, as well as a significant reduction of eotaxin, interleukin-4, and interleukin-1 beta in bronchoalveolar lavage fluid. These findings not only prove that NF-kappa B plays a critical role in the pathogenesis of allergic inflammation but also illustrate that inhibiting NF-kappa B could have therapeutic value in the treatment of asthma and potentially other chronic inflammatory lung diseases.