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Evaluation of transcriptomic responses in mouse larynx after cigarette smoke (CS) and electronic cigarette (E-Cigarette) exposures

ABSTRACT: Cigarette smoking is strongly associated with various laryngeal conditions, such as laryngitis, Reinke’s edema, laryngeal leukoplakia, and laryngeal cancer. Although E-Cigarettes have emerged as a prevalent alternative to traditional cigarettes, their effects on the larynx are not thoroughly characterized, and there is limited understanding of the molecular alterations induced by their aerosols. The objective of this study is to conduct a direct comparison of the laryngeal transcriptomic responses resulting from exposure to conventional CS and E-Cigarette aerosol. Utilizing high-throughput mRNA sequencing analysis, this research intends to identify both unique and overlapping molecular signatures associated with each form of exposure. The findings of this investigation will contribute to a deeper understanding of the implications of these tobacco products on laryngeal health and will serve as a valuable foundation for future studies in this domain.

ORGANISM(S): Mus musculus

PROVIDER: GSE294949 | GEO | 2026/04/15

REPOSITORIES: GEO

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Project description:Background: While electronic cigarette (ECIG) use is rapidly rising, their safety profile remains uncertain. The effects of tobacco cigarette (TCIG) smoke on bronchial airway epithelial gene-expression have provided insights into tobacco-related disease pathogenesis. Understanding the impact of electronic cigarettes (ECIGs) on airway gene-expression could provide insights into their potential long-term health effects. Objectives: We sought to compare the bronchial airway gene-expression profiles of former TCIG smokers now using ECIGs with the profiles of former and current TCIG smokers. Methods: We performed gene-expression profiling of bronchial epithelial cells collected from TCIG smokers not using ECIGs (n=21), former smokers using ECIGs (n=15), and current TCIG smokers not using ECIGs (n=9). We then compared our findings with previous studies of the effects of TCIG use on bronchial epithelium, as well an in vitro model of ECIG exposure. Results: Amongst 3,165 genes whose expression varied between the three study groups (q < 0.05), we identified 468 genes significantly altered in ECIG users relative to former smokers (p < 0.05). 79 of these genes were up or down-regulated concordantly between ECIG and TCIG. We did not detect ECIG-associated gene expression changes in known pathways associated with TCIG usage. Genes downregulated in ECIG users are enriched among the genes most downregulated by exposure of airway epithelium to ECIG vapor in vitro. Conclusions: TCIG exposure was associated with a larger number of airway gene-expression changes than with ECIG exposures. ECIGs induce both distinct and shared patterns of gene expression relative to TCIGs in the bronchial airway epithelium.

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