Prevalence studies of current smoking, among hospitalized COVID-19 patients, demonstrated an unexpectedly low prevalence among patients with COVID-19. The aim of the present study was to evaluate the effect of smoke from cigarettes on ACE-2 in bronchial epithelial cells. Normal bronchial epithelial cells (H292) were exposed to smoke by an air-liquid-interface (ALI) system and ACE-2 membrane protein expression was evaluated after 24 h from exposure. Our transcriptomics data analysis showed a significant selective reduction of membrane ACE-2 expression (about 25%) following smoking exposure. Interestingly, we observed a positive direct correlation between ACE-2 reduction and nicotine delivery. Furthermore, by stratifying GSE52237 as a function of ACE-2 gene expression levels, we highlighted 1,012 genes related to ACE-2 in smokers and 855 in non-smokers. Furthermore, we showed that 161 genes involved in the endocytosis process were highlighted using the online pathway tool KEGG. Finally, 11 genes were in common between the ACE-2 pathway in smokers and the genes regulated during endocytosis, while 12 genes with non-smokers. Interestingly, six in non-smokers and four genes in smokers were closely involved during the viral internalization process. Our data may offer a pharmaceutical role of nicotine as potential treatment option in COVID-19.
【저자키워드】 Nicotine, ACE-2, epithelial cells, cigarette, smoke, 【초록키워드】 COVID-19, Gene Expression, transcriptomics, smoking, Prevalence, membrane protein, Data analysis, pathway, membrane, correlation, expression, smoker, reduction, hospitalized COVID-19 patients, potential treatment option, bronchial epithelial cells, KEGG, selective, positive, offer, normal, involved, evaluated, demonstrated, regulated, bronchial epithelial cell, evaluate the effect, patients with COVID-19, 【제목키워드】 Model, interface, bronchial, role,