Effects of omalizumab and budesonide on markers of inflammation in human bronchial epithelial cells

Background: Many patients with asthma have an IgE-mediated allergic component to the disease. Omalizumab, a monoclonal anti-IgE antibody, has demonstrated clinical efficacy in patients with allergic asthma. The effects of omalizumab oil inflammation in asthma are not completely understood. Objectives: To evaluate the effects of omalizumab on allergen- and growth factor-stimulated proinflammatory cytokine and nitric oxide (NO) production in human bronchial epithelial cells (BECs) and to compare them to the effects of budesonide, a corticosteroid with known anti-inflammatory properties. Methods: Human BECs were stimulated in duplicate with interleukin 1 beta (IL-1 beta), 100 U/mL; ragweed, 10 mu g/mL; dust mite, 1,000 AU and epithelial growth factor, 40 ng/mL; and either 10(-7) M budesonide or 0.1 mu g/mL omalizumab in a 4% dust mite atopic serum medium for 6 and 24 hours in 5% carbon dioxide at 37 degrees C. Tumor necrosis factor alpha and transforming growth factor beta expression and production and IL-4, IL-13, and NO production were assayed using gene-specific messenger RNA or sensitive enzyme-linked immunosorbent assays. Results: Omalizumab inhibited the expression and of production proinflammatory cytokines and growth factor in antigen-stimulated BECs at 6 and 24 hours. Production of NO was inhibited at 6 hours and increased at 24 hours by omalizumab and budesonide. Conclusions: The effects of omalizumab were similar to those of budesonide. These results, consistent with previously reported evidence of anti-inflammatory effects of omalizumab, demonstrate that omalizumab may reduce airway inflammation and probably contributes to decreased airway remodeling in patients with asthma.