ArticleAmerican journal of physiology. Lung cellular and molecular physiology2025
The impact of electronic cigarettes on airway epithelial barrier integrity in preclinical mouse model.
Article in American journal of physiology. Lung cellular and molecular physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Electronic cigarette aerosols disrupt airway barrier function via MMP-dependent E-cadherin cleavage: findings from cell culture and murine models.Archives of toxicology · 2026Article
- Article
- Article
- Vaping versus smoking: a quest for long-term impact in a mouse model.BMC pulmonary medicine · 2025Article
- The respiratory epithelium in the era of vaping: insights fromEuropean respiratory review : an official journal of the European Respiratory Society · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
The increasing use of electronic cigarettes (e-cigs) among adolescents poses significant public health risks. This study investigates the impact of e-cigs on the airway epithelial barrier, focusing on apical junctional complexes (AJCs), including tight junctions (TJs) and adherens junctions (AJs). We hypothesized that e-cigs disrupt AJCs in a mouse model, leading to increased airway barrier permeability. C57BL/6 mice were exposed to 36 mg/mL e-cig aerosols (3 puffs/min) for 1 h daily over 4 days. Bronchoalveolar lavage (BAL) fluid analysis, lung inflammation assessment, immunohistochemistry (IHC) staining, Western blotting (WB), and permeability assays were performed to evaluate the structure and function of the airway barrier. E-cig-exposed mice showed weight loss and elevated serum cotinine levels. BAL fluid analysis revealed elevated white blood cells. Histological analysis confirmed lung inflammation, whereas IHC and WB showed significant AJC disruption. Notably, claudin-2 levels were elevated in e-cig-exposed mice compared with controls. Claudin-2, known for its role in promoting permeability in "leaky" epithelia, increased alongside decreases in other TJ components, signifying structural barrier impairment. After e-cig exposure, instilling fluorescein isothiocyanate (FITC)-dextran into the airway increased serum FITC-dextran levels, indicating enhanced barrier permeability. E-cig aerosol exposure disrupts airway epithelial barrier structure and function, primarily through the disassembly of TJs and AJs. These findings suggest potential pathways for further clinical investigation into the health risks of e-cig use.
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Registered trials
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