Cigarette smoke induce Epithelial-Derived Inflammation through activating autophagy via RAGE signaling in bronchial epithelial cells

Cigarette smoke (CS) is the critical risk of chronic obstructive pulmonary disease (COPD) characterized by the persistently abnormal inflammatory response. Airway epithelial cells are the front line of defense against inhaled toxin and pathogen. Recently, several evidences suggest that CS-stimulated inflammatory response via autophagy activation in the bronchial epithelial cell. Receptor for advanced glycation end products (RAGE) is a crucial inflammatory mediator in pulmonary diseases including COPD have been documented. In this study, we hypothesize that CSE induces epithelial-derived inflammation is associated with RAGE signaling pathway and autophagy. BEAS-2B and A549 human bronchial epithelial cells exposed to cigarette smoke extract. Inflammatory cytokines IL-6, IL-8, TNFα, MIG, IP-10, I-TAC were detected by quantitative real-time PCR. Autophagy was determined by flow cytometry, acridine orange staining. The expression of LC-3, Beclin1 and RAGE were by determined western blotting. Statistical analyses were performed using GraphPad Prism version 5.0. P-values