Aston Institute of Materials Research, School of Engineering and Applied Science, Aston University, Birmingham B4 7ET, United Kingdom.
School of Life and Health Sciences, Aston University, Birmingham B4 7ET, United Kingdom; Aston Medical Research Institute, Aston University, Birmingham B4 7ET, United Kingdom.
Toxicol In Vitro. 2018 Oct;52:255-264. doi: 10.1016/j.tiv.2018.06.020. Epub 2018 Jun 27.
Currently there is a lack of consensus on the possible adverse health effects of E-cigarettes (ECs). Important factors including cell model employed and exposure method determine the physiological relevance of EC studies. The present study aimed to evaluate EC cytotoxicity using a physiologically relevant in-vitro multicellular model of human airways. Human bronchial epithelial cells (CALU-3) and pulmonary fibroblasts (MRC-5) were co-cultured at air-liquid-interface for 11-14 days post which they were exposed to whole cigarette smoke (WCS) or EC vapour (ECV) at standard ISO-3308 regime for 7 m using a bespoke aerosol delivery system. ECV effects were further investigated at higher exposure times (1 h-6 h). Results showed that while WCS significantly reduced cell viability after 7 m, ECV decreased cell viability only at exposure times higher than 3 h. Furthermore, ECV caused elevated IL-6 and IL-8 production despite reduced cell viability. ECV exposure also produced a marked increase in oxidative stress. Finally, WCS but not ECV exposure induced caspase 3/7 activation, suggesting a caspase independent death of ECV exposed cells. Overall, our results indicate that prolonged ECV exposure (≥3 h) has a significant impact on pro-inflammatory mediators' production, oxidative stress and cell viability but not caspase 3/7 activity.
目前,对于电子烟(EC)可能对健康造成的不良影响还没有共识。细胞模型的选择和暴露方式等重要因素决定了 EC 研究的生理学相关性。本研究旨在使用人体气道的体外多细胞模型来评估 EC 的细胞毒性。在气道-液-界面共培养 11-14 天后,将人支气管上皮细胞(CALU-3)和肺成纤维细胞(MRC-5)暴露于标准 ISO-3308 条件下的全烟烟雾(WCS)或 EC 蒸汽(ECV)中 7 分钟,使用定制的气溶胶输送系统。进一步研究了更高暴露时间(1 小时-6 小时)下的 ECV 效应。结果表明,虽然 WCS 在 7 分钟后显著降低了细胞活力,但 ECV 仅在暴露时间超过 3 小时时才降低细胞活力。此外,尽管细胞活力降低,但 ECV 仍导致 IL-6 和 IL-8 的产生增加。ECV 暴露还产生了明显的氧化应激增加。最后,WCS 暴露而不是 ECV 暴露诱导了 caspase 3/7 的激活,这表明 ECV 暴露细胞的死亡与 caspase 无关。总体而言,我们的结果表明,长时间(≥3 小时)暴露于 ECV 对促炎介质的产生、氧化应激和细胞活力有显著影响,但对 caspase 3/7 活性没有影响。