The Nucleotide-Binding Oligomerization Domain–Like Receptor Family Pyrin Domain-Containing 3 Inflammasome Regulates Bronchial Epithelial Cell Injury and Proapoptosis after Exposure to Biomass Fuel Smoke
| Autor: | Xie Siming, Liu Xiaoyan, Liu Sheng-ming, Chen Qing, Chen Li, Luo Wenzhi, Li Wenlong, Huang ZhiHong |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
Male
0301 basic medicine Inflammasomes Clinical Biochemistry Apoptosis Pyrin domain Pulmonary Disease Chronic Obstructive 0302 clinical medicine Cell Movement Smoke Biomass education.field_of_study integumentary system Smoking Inflammasome Middle Aged Immunohistochemistry Up-Regulation Cell biology Cytokines Female Inflammation Mediators medicine.symptom medicine.drug Pulmonary and Respiratory Medicine Cell Survival Population Bronchi Inflammation Biology 03 medical and health sciences NLR Family Pyrin Domain-Containing 3 Protein medicine Humans education Molecular Biology Cell damage Aged Cell Proliferation Demography Cell growth Epithelial Cells Cell Biology medicine.disease Oxidative Stress 030104 developmental biology 030228 respiratory system Immunology Respiratory epithelium |
| Zdroj: | American Journal of Respiratory Cell and Molecular Biology. 55:815-824 |
| ISSN: | 1535-4989 1044-1549 |
| DOI: | 10.1165/rcmb.2016-0051oc |
| Popis: | The number of individuals in the population exposed to biomass fuel smoke (BS) is far greater than the number of cigarette smokers. About 20% of cigarette smokers develop chronic obstructive pulmonary disease (COPD) due to smoke-induced irreversible damage and sustained inflammation of the airway epithelium. However, the role of BS in COPD pathogenesis remains to be elucidated. In this study, we investigated the expression of nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing (NLRP) 3 and caspase-1 in the bronchial epithelium from patients with COPD, and further determined the specific role of the NLRP3 inflammasome in bronchial epithelium injury using two in vitro models (BS and cigarette smoke [CS]) in the human bronchial epithelial (HBE) cell line (16HBE). After exposure to BS and CS, the release of damage-associated molecular patterns, the transcriptional and translational up-regulation of NLRP3, and the activation of caspase-1 were observed in cells at different time points. Because IL-1β secretion was dependent on the NLRP3 inflammasome, we assessed CXCL-8 production in response to smoke. Using a transwell migration assay in which 16HBE cells and human alveolar macrophages were cocultured, we showed that smoke-induced NLRP3 activation in 16HBE cells increased the migration of human alveolar macrophages. When the NLRP3 expression was silenced, the average migration distance of 16HBE was increased in scratch assay, because the activation of NLRP3 induced apoptosis by the p53-Bax mitochondrial pathway in the smoke-induced response. These results demonstrate the importance of the NLRP3 inflammasome in mediating BS- and CS-induced HBE cell damage and proapoptosis. |
| Databáze: | OpenAIRE |
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