Acute exposure to e-cigarettes causes inflammation and pulmonary endothelial oxidative stress in nonsmoking, healthy young subjects
Acute exposure to e-cigarettes causes inflammation and pulmonary endothelial oxidative stress in nonsmoking, healthy young subjects
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DOI：
10.1152/ajplung.00110.2019
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发表时间：
2019-08-01
影响因子：
4.9
通讯作者：
Wehrli, Felix W.
中科院分区：
文献类型：
--
作者：
Chatterjee, Shampa;Tao, Jian-Qin;Wehrli, Felix W.
到目前为止，还没有研究过非吸烟者吸入电子烟（e-cig）的影响。本研究旨在评估雾化吸入非尼古丁化电子烟的急性反应，包括氧化应激和人肺微血管内皮细胞（HPMVEC）的内皮激活指数。对10名未吸烟的健康受试者（平均年龄+/- SD = 28.7 +/- 5.5岁）进行电子烟激发，随后监测其血清中的炎症标志物[C-反应蛋白（CRP）和可溶性细胞间粘附分子（sICAM）]和一氧化氮代谢物（NOx）。循环血清对血管网的氧化应激和炎症负荷也通过测量HPMVEC上活性氧（ROS）产生和ICAM-1表达的诱导来评估。结果表明，雾化吸入电子烟后，血清氧化应激和炎症指标明显升高（P < 0.05），在吸入后1-2 h达到高峰，6 h恢复到基线水平。血清（ICAM-1和ROS）的循环负荷在2小时显著增加，并在电子烟激发后6小时恢复至基线值。发现HPMVEC的ROS产生通过NADPH氧化酶2（NOX 2）途径的活化而发生。这些发现表明，即使在没有尼古丁的情况下，急性电子烟气雾吸入也会导致氧化应激和炎症的短暂增加。这可以通过促进氧化应激和免疫细胞粘附而对血管内皮网络产生不利影响。因此，电子烟吸入有可能导致血管病变的发生。
The effects of e-cigarette (e-cig) aerosol inhalation by nonsmokers have not been examined to date. The present study was designed to evaluate the acute response to aerosol inhalation of non-nicotinized e-cigarettes in terms of oxidative stress and indices of endothelial activation in human pulmonary microvascular endothelial cells (HPMVEC). Ten smoking-naive healthy subjects (mean age +/- SD = 28.7 +/- 5.5 yr) were subjected to an e-cig challenge, following which their serum was monitored for markers of inflammation [C-reactive protein (CRP) and soluble intercellular adhesion molecule (sICAM)] and nitric oxide metabolites (NOx). The oxidative stress and inflammation burden of the circulating serum on the vascular network was also assessed by measuring reactive oxygen species (ROS) production and induction of ICAM-1 expression on HPMVEC. Our results show that serum indices of oxidative stress and inflammation increased significantly (P < 0.05 as compared with baseline), reaching a peak at approximately 1-2 h post-e-cig aerosol inhalation and returning to baseline levels at 6 h. The circulatory burden of the serum (ICAM-1 and ROS) increased significantly at 2 h and returned to baseline values 6 h post-e-cig challenge. ROS production by HPMVEC was found to occur via activation of the NADPH oxidase 2 (NOX2) pathways. These findings suggest that even in the absence of nicotine, acute e-cig aerosol inhalation leads to a transient increase in oxidative stress and inflammation. This can adversely affect the vascular endothelial network by promoting oxidative stress and immune cell adhesion. Thus e-cig inhalation has the potential to drive the onset of vascular pathologies.