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.

中文翻译：

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香烟烟雾和电子香烟可差异性激活支气管上皮细胞

电子烟（ECIG）的使用正在增加，但是人们对ECIG蒸气对诸如炎症或宿主防御之类的细胞过程的影响的了解却很少。本研究的目的是比较传统香烟（TCIG）和ECIG暴露对宿主防御，炎症以及细胞系和原代分化的人气道上皮细胞（pHBE）的细胞活化的急性作用。我们将pHBEs和一些细胞系暴露于TCIG烟或ECIG蒸汽中。确定上皮宿主防御和屏障完整性。通过基因表达阵列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验证了几种候选基因的表达。细菌杀灭，与对照样品相比，ECIG-蒸气不影响屏障的完整性和抗菌肽的表达。相反，TCIG对主机防御产生了负面影响，并显着降低了屏障的完整性。此外，ECIG暴露可显着诱导Calu-3细胞分泌IL-8，但对NCI-H292或原代细胞无影响。基于阵列分析的基因表达从ECIG和暴露于室内空气的样品中区分了TCIG暴露的细胞。在ECIG暴露的细胞和TCIG处理的细胞之间，宿主防御和炎症基因的转录组模式明显不同。与TCIG相比，ECIGs对上皮细胞的总体作用较小，并且ECIG蒸气不影响宿主防御。尽管如此，尽管急性暴露于ECIG蒸汽会引起炎症和S100蛋白的表达，