Department of Internal Medicine V - Pulmonology, Allergology and Critical Care Medicine, Saarland University, D-66421, Homburg, Germany.
Clinical Bioinformatics, Saarland University, University Hospital, 66123, Saarbrücken, Germany.
Respir Res. 2020 Mar 12;21(1):67. doi: 10.1186/s12931-020-1317-2.
The use of electronic cigarettes (ECIGs) is increasing, but the impact of ECIG-vapor on cellular processes like inflammation or host defense are less understood. The aim of the present study was to compare the acute effects of traditional cigarettes (TCIGs) and ECIG-exposure on host defense, inflammation, and cellular activation of cell lines and primary differentiated human airway epithelial cells (pHBE).
We exposed pHBEs and several cell lines to TCIG-smoke or ECIG-vapor. Epithelial host defense and barrier integrity were determined. The transcriptome of airway epithelial cells was compared by gene expression array analysis. Gene interaction networks were constructed and differential gene expression over all groups analyzed. The expression of several candidate genes was validated by qRT-PCR.
Bacterial killing, barrier integrity and the expression of antimicrobial peptides were not affected by ECIG-vapor compared to control samples. In contrast, TCIGs negatively affected host defense and reduced barrier integrity in a significant way. Furthermore ECIG-exposure significantly induced IL-8 secretion from Calu-3 cells but had no effect on NCI-H292 or primary cells. The gene expression based on array analysis distinguished TCIG-exposed cells from ECIG and room air-exposed samples.
The transcriptome patterns of host defense and inflammatory genes are significantly distinct between ECIG-exposed and TCIG-treated cells. The overall effects of ECIGs on epithelial cells are less in comparison to TCIG, and ECIG-vapor does not affect host defense. Nevertheless, although acute exposure to ECIG-vapor induces inflammation, and the expression of S100 proteins, long term in vivo data is needed to evaluate the chronic effects of ECIG use.
电子烟的使用正在增加，但电子烟蒸汽对炎症或宿主防御等细胞过程的影响还不太清楚。本研究的目的是比较传统香烟（TCIG）和电子烟暴露对细胞系和原代分化的人气道上皮细胞（pHBE）宿主防御、炎症和细胞激活的急性影响。
我们将 pHBE 和几种细胞系暴露于 TCIG 烟雾或电子烟蒸汽中。测定上皮宿主防御和屏障完整性。通过基因表达谱分析比较气道上皮细胞的转录组。构建基因相互作用网络，并分析所有组的差异基因表达。通过 qRT-PCR 验证了几个候选基因的表达。
与对照样品相比，电子烟蒸汽对细菌杀伤、屏障完整性和抗菌肽表达没有影响。相比之下，TCIG 以显著方式负性影响宿主防御并降低屏障完整性。此外，电子烟暴露显著诱导 Calu-3 细胞中 IL-8 的分泌，但对 NCI-H292 或原代细胞没有影响。基于阵列分析的基因表达将 TCIG 暴露的细胞与电子烟和室内空气暴露的样本区分开来。
宿主防御和炎症基因的转录组模式在电子烟暴露和 TCIG 处理的细胞之间存在显著差异。与 TCIG 相比，电子烟对上皮细胞的总体影响较小，电子烟蒸汽不会影响宿主防御。然而，尽管电子烟蒸汽的急性暴露会引起炎症和 S100 蛋白的表达，但需要进行体内长期数据评估电子烟使用的慢性影响。
