E-cigarette Vapor Extract Alters Human Eosinophil Gene Expression in an Effect Mediated by Propylene glycol, Glycerin, and Nicotine

E-cigarette use (vaping) has become widespread, and its effects on airway inflammation and disease are not fully delineated. E-cigarette vapor extract (EVE) profoundly affects neutrophil function. We hypothesized that EVE also alters eosinophil function and thus could impact allergic airways disease. We employed RNA-sequencing to measure the ex vivo effect of EVE components on human eosinophil transcription. Eosinophils from 7 non-vaping subjects without asthma were isolated by negative selection from venous blood. Cells were incubated for 48 hours with EVE consisting of glycerin, propylene glycol and nicotine (EVE+), EVE without nicotine (“EVE-”), Extract Buffer (EB), and untreated media. Bulk RNA-sequencing was performed. Principal component analysis revealed that the EVE+ and EVE- conditions clustered closely together. Differential gene expression analysis revealed a “negative regulation of interferon gamma production” and “apoptotic mitochondrial changes” pathways for genes upregulated in EVE- samples and a down regulation of “inflammatory response” and “chemokine signaling” in comparison to the EB control condition. 93 genes were differentially expressed genes between EVE+ and EVE-, indicating a relatively small effect of nicotine on eosinophil gene expression. These results demonstrate that EVE significantly alters eosinophil gene expression, predominantly mediated by propylene glycol and glycerin rather than by nicotine. This study motivates further research into the pathogenic effects of vaping on airway eosinophils and allergic airways disease.