Chlamydophila pneumoniae Triggers Release of CCL20 and Vascular Endothelial Growth Factor from Human Bronchial Epithelial Cells Through Enhanced Intracellular Oxidative Stress and MAPK Activation

摘要

Background Chlamydophila pneumoniae may contribute to the pathogenesis of asthmatic airway inflammation through chemical mediators secreted by C. pneumoniae-infected bronchial epithelial cells (BECs). Recently, CCL20 and vascular endothelial growth factor (VEGF) were reported to be released from BECs and to play a role in the pathogenesis of asthma.