Zhou Guojun, Xiao Weiqiang, Xu Chengyun, Hu Yajun, Wu Xiaokai, Huang Fangfang, Lu Xinbo, Shi Chunyun, Wu Ximei
Technological Center of China Tobacco Zhejiang Industrial Co., LTD., 118 Kehai Road, Hangzhou, Zhejiang Province 310024 China.
Department of Pharmacology, School of Medicine, Zhejiang University, 866 Yuhangtang Road, Hangzhou, 310058 China.
Tob Induc Dis. 2016 Jul 19;14:24. doi: 10.1186/s12971-016-0089-4. eCollection 2016.
Interleukin-8 (IL-8) functions as a major chemoattractant and plays pivotal roles in the initiation and development of chronic obstructive pulmonary disease (COPD), and tobacco smoke is a most risk factor contributing to the development of COPD. Hence, we have screened some of the tobacco smoke-derived chemical compounds that potentially induce the production of IL-8 in human bronchial epithelium, 16HBE cells.
Twenty-eight hazardous smoke components belonging to 9 classes including nicotine, ammonia, aromatic amines, polycyclic aromatic hydrocarbons, phenols, carbonyls, hydrocyanic acid, nitrosamines and other volatile organics were used in the experiments. Proliferation of 16HBE cells was determined by cell counting kit-8 kit, luciferase activity was measured in IL-8 reporter gene-expressing 16HBE cells, and IL-8 levels in culture supernatants were quantified by enzyme-linked immunosorbent assay.
At the non-toxic dosages, chemical compounds belonging to nicotine, aromatic amines, benzopyrene, phenols, aldehydes, and some other volatile organics dose-dependently increased IL-8 reporter gene expression. Consistently, the representative compounds belonging to nicotine, aromatic amines, benzopyrene, phenols, aldehydes, and some other volatile organics significantly and dose-dependently increased IL-8 levels in the culture supernatants of 16HBE cells, among these compounds, benzopyrene is a most potent stimulator for inducing IL-8 production.
The present study has identified particular tobacco smoke constituents responsible for inducing the IL-8 production in human bronchial epithelium, which might help shed light on the pathogenesis of tobacco smoke-induced COPD.
白细胞介素-8（IL-8）作为一种主要的趋化因子，在慢性阻塞性肺疾病（COPD）的发生和发展中起关键作用，而烟草烟雾是导致COPD发生的最重要危险因素。因此，我们筛选了一些烟草烟雾衍生的化合物，这些化合物可能会诱导人支气管上皮细胞16HBE细胞产生IL-8。
实验使用了属于9类的28种有害烟雾成分，包括尼古丁、氨、芳香胺、多环芳烃、酚类、羰基化合物、氢氰酸、亚硝胺和其他挥发性有机物。通过细胞计数试剂盒-8试剂盒测定16HBE细胞的增殖情况，在表达IL-8报告基因的16HBE细胞中测量荧光素酶活性，并通过酶联免疫吸附测定法定量培养上清液中的IL-8水平。
在无毒剂量下，属于尼古丁、芳香胺、苯并芘、酚类、醛类和其他一些挥发性有机物的化合物剂量依赖性地增加IL-8报告基因的表达。同样，属于尼古丁、芳香胺、苯并芘、酚类、醛类和其他一些挥发性有机物的代表性化合物显著且剂量依赖性地增加了16HBE细胞培养上清液中的IL-8水平，在这些化合物中，苯并芘是诱导IL-8产生的最有效刺激物。
本研究确定了导致人支气管上皮细胞产生IL-8的特定烟草烟雾成分，这可能有助于阐明烟草烟雾诱导的COPD的发病机制。
