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

摘要: 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 asthma. The effects of omalizumab on inflammation are not completely understood. Objectives To evaluate allergen- and growth factor-stimulated proinflammatory cytokine nitric oxide (NO) production human bronchial epithelial cells (BECs) compare them budesonide, corticosteroid known anti-inflammatory properties. Methods Human BECs were stimulated duplicate interleukin 1β (IL-1β), 100 U/mL; ragweed, 10 μg/mL; dust mite, 1,000 AU; factor, 40 ng/mL; either −7 M budesonide or 0.1 μg/mL 4% mite atopic serum medium for 6 24 hours 5% carbon dioxide at 37°C. Tumor necrosis factor α transforming β expression IL-4, IL-13, NO assayed using gene-specific messenger RNA sensitive enzyme-linked immunosorbent assays. Results Omalizumab inhibited cytokines antigen-stimulated hours. Production was increased by budesonide. Conclusions similar those These results, consistent previously reported evidence omalizumab, demonstrate that may reduce airway probably contributes decreased remodeling