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<p>Cigarette smoke is the leading cause of lung diseases including chronic bronchitis and chronic obstructive pulmonary disease (COPD). While harmful effects of cigarette smoke on lung epithelial function are well established, the consequences of inhalation of aerosols from e-cigarettes are less clear and disputed. In this study, human lung adenocarcinoma epithelial cells (Calu-3) were treated with extracts of cigarette smoke (CSE) or e-cigarette vapor (EVE) and comparatively analyzed for barrier function and integrity as well as for mRNA and protein expression of components forming the apical junctional complex (AJC). In addition, potential proinflammatory and genotoxic effects were investigated. Our results clearly demonstrate that CSE induced considerable disruption of the epithelial barrier leading to hyperpermeability and reduced protein expression of AJC proteins, especially of claudin-1. In addition, exposure of cells to CSE induced pronounced proinflammatory effects and increased DNA double strand breaks. By contrast, EVE, even if applied undiluted, neither affected functional nor structural parameters. In summary, on the basis of our results obtained with the Calu-3 in vitro model, we propose that e-cigarette vapor may exert less harmful effects on lung epithelial cells compared to cigarette smoke.</p>

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Tobacco smoke but not e-cigarette vapor induces epithelial barrier disruption, inflammation, and DNA damage in human Calu-3 cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月9日

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  • Bernd Mayer,
  • Alexander Kollau,
  • Wolfgang Kappaun,
  • Katrin Rauchegger,
  • Gerald Wölkart,
  • Alexander Toedtling,
  • Astrid Schrammel

摘要

Cigarette smoke is the leading cause of lung diseases including chronic bronchitis and chronic obstructive pulmonary disease (COPD). While harmful effects of cigarette smoke on lung epithelial function are well established, the consequences of inhalation of aerosols from e-cigarettes are less clear and disputed. In this study, human lung adenocarcinoma epithelial cells (Calu-3) were treated with extracts of cigarette smoke (CSE) or e-cigarette vapor (EVE) and comparatively analyzed for barrier function and integrity as well as for mRNA and protein expression of components forming the apical junctional complex (AJC). In addition, potential proinflammatory and genotoxic effects were investigated. Our results clearly demonstrate that CSE induced considerable disruption of the epithelial barrier leading to hyperpermeability and reduced protein expression of AJC proteins, especially of claudin-1. In addition, exposure of cells to CSE induced pronounced proinflammatory effects and increased DNA double strand breaks. By contrast, EVE, even if applied undiluted, neither affected functional nor structural parameters. In summary, on the basis of our results obtained with the Calu-3 in vitro model, we propose that e-cigarette vapor may exert less harmful effects on lung epithelial cells compared to cigarette smoke.