Quantitative proteomics study reveals cross-talk between autophagy and inflammation induced by cigarette smoke in airway

Introduction: Cigarette smoke (CS) is an important risk factor for the development of airway inflammation. Autophagy can be induced by CS, while the role of autophagy in airway inflammation induced by CS was still unclear. We sought to determine the the role of autophagy in airway inflammation induced by CS using systems-level analysis by amino acids in cell culture (SILAC)-based quantitative proteomics. Methods: SILAC-labeled human lung mucoepidermoid cells (NCI-H292) was exposed to cigarette smoke extract for 24h, and then was used to identify the differentially expressed proteins. In order to validate the results in vivo, rats were exposed to CS for 4 weeks. Besides the analysis of bronchoalveolar lavage fluid (BALF) and histological changes, immunohistochemistry and western blot validate the selected proteins. Autophagy was observed by electron microscope (EM). Results: Three proteins associated with autophagy were significantly up-regulated after CS exposure in NCI-H292 cell (p Conclusions: Autophagy may play a role in airway inflammation induced by CS.