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Nicotine-Free e-Cigarette Vapor Exposure Stimulates IL6 and Mucin Production in Human Primary Small Airway Epithelial Cells.
Journal of Inflammation Research ( IF 4.2 ) Pub Date : 2020-04-16 , DOI: 10.2147/jir.s244434
Shaan Gellatly 1 , Nicole Pavelka 1 , Taylor Crue 1 , Kelly S Schweitzer 1 , Brian J Day 1 , Elysia Min 1 , Mari Numata 1 , Dennis R Voelker 1 , April Scruggs 1 , Irina Petrache 1 , Hong Wei Chu 1
Affiliation  

Purpose: Electronic cigarettes (e-cigs) are relatively new devices that allow the user to inhale a heated and aerosolized solution. At present, little is known about their health effects in the human lung, particularly in the small airways (< 2 mm in diameter), a key site of airway obstruction and destruction in chronic obstructive pulmonary disease and other acute and chronic lung conditions. The aim of this study was to investigate the effect of e-cigarettes on human distal airway inflammation and remodeling.
Methods: We isolated primary small airway epithelial cells from donor lungs without known lung disease. Small airway epithelial cells were cultured at air–liquid interface and exposed to 15 puffs vapor obtained by heating a commercially available e-cigarette solution (e-vapor) with or without nicotine. After 24 hrs of e-vapor exposure, basolateral and apical media as well as cell lysates were collected to measure the pleiotropic cytokine interleukin 6 (IL6) and MUC5AC, one of the major components in mucus.
Results: Unlike the nicotine-containing e-vapor, nicotine-free e-vapor significantly increased the amount of IL6, which was coupled with increased levels of intracellular MUC5AC protein. Importantly, a neutralizing IL6 antibody (vs an IgG isotype control) significantly inhibited the production of MUC5AC induced by nicotine-free e-vapor.
Conclusion: Our results suggest that human small airway epithelial cells exposed to nicotine-free e-vapor increase the inflammatory response and mucin production, which may contribute to distal lung airflow limitation and airway obstruction.

Keywords: electronic cigarette, small airway epithelial cells, inflammation, interleukin 6, mucus


中文翻译:


不含尼古丁的电子烟蒸汽暴露刺激人原代小气道上皮细胞产生 IL6 和粘蛋白。



用途:电子烟(e-cigs)是相对较新的设备,允许用户吸入加热的雾化溶液。目前,人们对它们对人类肺部健康的影响知之甚少,特别是在小气道(直径<2毫米)中,小气道是慢性阻塞性肺病和其他急慢性肺部疾病中气道阻塞和破坏的关键部位。本研究的目的是调查电子烟对人类远端气道炎症和重塑的影响。

方法:我们从没有已知肺部疾病的供体肺中分离出原代小气道上皮细胞。小气道上皮细胞在气液界面培养,并暴露于通过加热含有或不含尼古丁的市售电子烟​​溶液(电子蒸气)获得的蒸气中,并暴露于 15 口蒸气中。电子蒸汽暴露 24 小时后,收集基底外侧和顶端介质以及细胞裂解物,以测量多效细胞因子白细胞介素 6 (IL6) 和 MUC5AC(粘液中的主要成分之一)。

结果:与含尼古丁的电子烟不同,不含尼古丁的电子烟显着增加了 IL6 的量,同时细胞内 MUC5AC 蛋白的水平也增加了。重要的是,中和性 IL6 抗体(相对于 IgG 同型对照)显着抑制由不含尼古丁的电子烟诱导的 MUC5AC 的产生。

结论:我们的结果表明,暴露于不含尼古丁的电子蒸汽的人小气道上皮细胞会增加炎症反应和粘蛋白的产生,这可能导致远端肺气流受限和气道阻塞。


关键词:电子烟, 小气道上皮细胞, 炎症, 白细胞介素6, 粘液
更新日期:2020-04-16
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