Cigarette smoke extract induces pyroptosis in human bronchial epithelial cells through the ROS/NLRP3/caspase-1 pathway

• DOI: 10.1016/j.lfs.2021.119090
• Publication Date: 2021-01-18T04:55:10Z
• Authors: Meng-Yu Zhang; Ying-Xiao Jiang; Yi-Can Yang; Jian-Yu Liu; Chen Huo; Xiu-Li Ji; Yi-Qing Qu
• Keywords: Pyroptosis

Pyroptosis and inflammation are involved in the development of chronic obstructive pulmonary disease (COPD). However, cigarette smoke-mediated mechanism COPD remains unclear. In this study, we aimed to investigate role nucleotide-binding domain-like receptor protein-3 (NLRP3) inflammasome-mediated pyroptosis death human bronchial epithelial (HBE) cells after smoke extract (CSE) exposure.The protein level NLRP3 lung tissue was measured exposure vivo. vitro, HBE were treated with CSE. Subsequently, activity caspase-1, lactate dehydrogenase (LDH) release, release interleukin (IL)-1β expression levels measured. The involvement reactive oxygen species (ROS) also explored.After CSE, increased LDH, transcriptional translational upregulation NLRP3, caspase-1 levels, enhanced IL-1β IL-18 observed 16HBE cells. addition, required activate caspase-1. Our results suggested that pre-stimulated a inhibitor, or using siRNA silence expression, caused decrease pyroptosis.CSE induced contributed through ROS/NLRP3/caspase-1 pathway inflammasome participates CSE-induced cell damage pyroptosis, which could provide new insights into COPD.