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Single-cell transcriptomics identifies altered neutrophil dynamics and accentuated T-cell cytotoxicity in tobacco -flavored e-cigarette -exposed mouse lungs

ABSTRACT: E-cigarettes (e-cigs) are a public health concern for young adults due to evidence for increased oxidative stress, lipid dysfunction, and inflammation. Yet an extensive study defining the cell-specific alterations on exposure to flavored e-cigs remains elusive. To understand the immunological lung landscape upon exposure to flavored e-cig (mango-, menthol- or tobacco-flavor) aerosols we performed single cell RNA sequencing (scRNA seq).

ORGANISM(S): Mus musculus

PROVIDER: GSE263903 | GEO | 2026/02/01

REPOSITORIES: GEO

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Genome-wide occupancy of H3K27me3 in human gingival mesenchymal and periodontal ligament stem cells in response to Electronic-cigarette

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A 6-month systems toxicology inhalation study in ApoE−/− mice demonstrates reduced cardiovascular effects of E-vapor aerosols compared to cigarette smoke.

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Structural, Functional and Molecular Impact on the Cardiovascular System in ApoE-/- Mice Exposed to Aerosol from modified risk tobacco products, the Carbon Heated Tobacco Product 1.2 and the Tobacco Heating System 2.2 compared to Cigarette Smoke effects (miRNA data).

Project description:AIM: To investigate the molecular, structural, and functional impact of aerosols from two heat-not-burn-based MRTPs, the Carbon Heated Tobacco Product (CHTP) 1.2 and Tobacco Heating System (THS) 2.2, compared with that of cigarette mainstream smoke (CS) on the cardiovascular system of ApoE-/- mice. METHOD: Female ApoE-/- mice were exposed to aerosols from THS 2.2 and CHTP 1.2 or to CS from 3R4F for up to 6 months at matching nicotine concentrations. A cessation and a switching group (3 months exposure to 3R4F CS followed by filtered air or CHTP 1.2 for 3 months) were included. Cardiovascular effects were investigated using echocardiography, histopathology, immunohistochemistry, and transcriptomics. RESULTS: Continuous exposure to aerosols from CHTP 1.2 and THS 2.2 did not affect the atherosclerosis progression, heart function, left ventricular structure and cardiovascular transcriptome. Exposure to CS from 3R4F triggered atherosclerosis progression, reduced systolic ejection fraction and fractional shortening, caused heart left ventricle hypertrophy and initiated significant dysregulation in the transcriptomes of the heart ventricle and thoracic aorta. Importantly, smoking cessation and switching to CHTP 1.2 aerosol similarly improved the structural, functional, and molecular changes caused by 3R4F CS. CONCLUSION: Exposure to aerosols from CHTP 1.2 and THS 2.2 lacked most of the CS exposure-related functional, structural and molecular effects. Smoking cessation or switching to CHTP 1.2 aerosol caused a similar recovery from the 3R4F CS effect in the ApoE-/- model with no further acceleration of plaque progression beyond the aging-related rate.

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