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Cigarette smoke extract induces pyroptosis in human bronchial epithelial cells through the ROS/NLRP3/caspase-1 pathway.
Life Sci. 2021 Mar 15; 269:119090.LS

Abstract

AIMS

Pyroptosis and inflammation are involved in the development of chronic obstructive pulmonary disease (COPD). However, the cigarette smoke-mediated mechanism of COPD remains unclear. In this study, we aimed to investigate the role of nucleotide-binding domain-like receptor protein-3 (NLRP3) inflammasome-mediated pyroptosis in the death of human bronchial epithelial (HBE) cells after cigarette smoke extract (CSE) exposure.

MAIN METHODS

The protein level of NLRP3 in lung tissue was measured after cigarette smoke exposure in vivo. In vitro, HBE cells were treated with CSE. Subsequently, the activity of caspase-1, lactate dehydrogenase (LDH) release, release of interleukin (IL)-1β and NLRP3 expression levels were measured. The involvement of reactive oxygen species (ROS) was also explored.

KEY FINDINGS

After exposure to CSE, increased release of LDH, the transcriptional and translational upregulation of NLRP3, the caspase-1 activity levels, and enhanced IL-1β and IL-18 release were observed in 16HBE cells. In addition, NLRP3 was required to activate the caspase-1. Our results suggested that pre-stimulated of 16HBE with a caspase-1 inhibitor, or using NLRP3 siRNA to silence NLRP3 expression, also caused the decrease of IL-1β release and pyroptosis.

SIGNIFICANCES

CSE induced inflammation and contributed to pyroptosis through the ROS/NLRP3/caspase-1 pathway in 16HBE cells. The NLRP3 inflammasome participates in CSE-induced HBE cell damage and pyroptosis, which could provide new insights into COPD.

Authors+Show Affiliations

Department of Pulmonary and Critical Care Medicine, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250012, China.Department of Pulmonary and Critical Care Medicine, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250012, China.Department of Pulmonary and Critical Care Medicine, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250012, China.Department of Pulmonary and Critical Care Medicine, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250012, China.Department of Pulmonary and Critical Care Medicine, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250012, China.Department of Pulmonary Disease, Jinan Traditional Chinese Medicine Hospital, Jinan 250012, China.Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Jinan 250012, China. Electronic address: quyiqing@sdu.edu.cn.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

33465393

Citation

Zhang, Meng-Yu, et al. "Cigarette Smoke Extract Induces Pyroptosis in Human Bronchial Epithelial Cells Through the ROS/NLRP3/caspase-1 Pathway." Life Sciences, vol. 269, 2021, p. 119090.
Zhang MY, Jiang YX, Yang YC, et al. Cigarette smoke extract induces pyroptosis in human bronchial epithelial cells through the ROS/NLRP3/caspase-1 pathway. Life Sci. 2021;269:119090.
Zhang, M. Y., Jiang, Y. X., Yang, Y. C., Liu, J. Y., Huo, C., Ji, X. L., & Qu, Y. Q. (2021). Cigarette smoke extract induces pyroptosis in human bronchial epithelial cells through the ROS/NLRP3/caspase-1 pathway. Life Sciences, 269, 119090. https://doi.org/10.1016/j.lfs.2021.119090
Zhang MY, et al. Cigarette Smoke Extract Induces Pyroptosis in Human Bronchial Epithelial Cells Through the ROS/NLRP3/caspase-1 Pathway. Life Sci. 2021 Mar 15;269:119090. PubMed PMID: 33465393.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cigarette smoke extract induces pyroptosis in human bronchial epithelial cells through the ROS/NLRP3/caspase-1 pathway. AU - Zhang,Meng-Yu, AU - Jiang,Ying-Xiao, AU - Yang,Yi-Can, AU - Liu,Jian-Yu, AU - Huo,Chen, AU - Ji,Xiu-Li, AU - Qu,Yi-Qing, Y1 - 2021/01/16/ PY - 2020/10/16/received PY - 2021/01/07/revised PY - 2021/01/12/accepted PY - 2021/1/20/pubmed PY - 2021/2/27/medline PY - 2021/1/19/entrez KW - Cigarette smoke extract KW - Human bronchial epithelial cells KW - NLRP3/caspase-1 inflammasome KW - Pyroptosis KW - ROS SP - 119090 EP - 119090 JF - Life sciences JO - Life Sci VL - 269 N2 - AIMS: Pyroptosis and inflammation are involved in the development of chronic obstructive pulmonary disease (COPD). However, the cigarette smoke-mediated mechanism of COPD remains unclear. In this study, we aimed to investigate the role of nucleotide-binding domain-like receptor protein-3 (NLRP3) inflammasome-mediated pyroptosis in the death of human bronchial epithelial (HBE) cells after cigarette smoke extract (CSE) exposure. MAIN METHODS: The protein level of NLRP3 in lung tissue was measured after cigarette smoke exposure in vivo. In vitro, HBE cells were treated with CSE. Subsequently, the activity of caspase-1, lactate dehydrogenase (LDH) release, release of interleukin (IL)-1β and NLRP3 expression levels were measured. The involvement of reactive oxygen species (ROS) was also explored. KEY FINDINGS: After exposure to CSE, increased release of LDH, the transcriptional and translational upregulation of NLRP3, the caspase-1 activity levels, and enhanced IL-1β and IL-18 release were observed in 16HBE cells. In addition, NLRP3 was required to activate the caspase-1. Our results suggested that pre-stimulated of 16HBE with a caspase-1 inhibitor, or using NLRP3 siRNA to silence NLRP3 expression, also caused the decrease of IL-1β release and pyroptosis. SIGNIFICANCES: CSE induced inflammation and contributed to pyroptosis through the ROS/NLRP3/caspase-1 pathway in 16HBE cells. The NLRP3 inflammasome participates in CSE-induced HBE cell damage and pyroptosis, which could provide new insights into COPD. SN - 1879-0631 UR - https://www.unboundmedicine.com/medline/citation/33465393/Cigarette_smoke_extract_induces_pyroptosis_in_human_bronchial_epithelial_cells_through_the_ROS/NLRP3/caspase_1_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(21)00075-8 DB - PRIME DP - Unbound Medicine ER -