Cigarette smoke triggers inflammation mediated by autophagy in BEAS-2B cells.

Cigarette smoking, as an individual consumption habit, is associated with a variety of related diseases. Exposure of cigarette smoke was reported to induce autophagy and inflammation in experimental animals and humans. However, the toxicity mechanism of cigarette smoke in organisms has not been entirely investigated. In this present study, we studied the role of autophagy played in the inflammation caused by cigarette smoke in human bronchial epithelial cells (BEAS-2B), as well as the role of the phosphatidylinositol 3-kinase (PI3K) signaling pathway and the mitogen-activated protein kinase (MAPK) signaling pathways underlying autophagy and inflammation. We found that cigarette smoke induced autophagy and inflammation in BEAS-2B, and the blockage of autophagy significantly reduced the release levels of IL-1β, IL-6 and IL-8 in BEAS-2B exposed to cigarette smoke for 24 h. Cigarette smoke downregulated the activity of PI3K/Akt/mTOR pathway and elevated the activity of MAPK pathways. Pretreatment of autophagic inhibitor could inhibit autophagy and the activity of JNK and p38 pathways. These results suggested that cigarette smoke-induced autophagy triggered inflammation through the activation of JNK and p38 pathways, which might contribute to understanding the adverse outcome pathways induced by cigarette smoke exposure and provide the information about the risk assessment of tobacco products.