Vaping versus smoking: a quest for long-term impact in a mouse model.

Smokers consider that electronic cigarettes are safer than tobacco and are marketed as safe products. Nevertheless, reports show the exposure to high levels of electronic cigarette aerosols (ECA) activates lung cells and triggers inflammation and structural alterations after chronic exposure. In order to assess the potential harmful long term effect of exposure to ECA, we investigated in mice, its effect on lung and systemic inflammation as well as on lung function. To reproduce closely the situation frequently encountered in human, we exposed mice during 1 h/day during 3 or 6 months with two levels of electronic cigarette power in comparison with mice exposed to cigarette smoke (CS). Lung and systemic inflammation was evaluated by measuring cell recruitment and activation or cytokine concentrations. Respiratory function and lung transcriptome and structure were also measured. Our data revealed that chronic exposure to moderate levels of ECA increased specifically lung inflammation, these effects being characterized by the mobilization of conventional dendritic cells in the BAL and the recruitment of T cells in the lungs and by the early secretion of IL-22. Surprisingly, there is no strong overlap between the impact of both ECA and CS exposure on lung transcriptome. Modulation of pro-inflammatory pathways are limited to mice exposed to low power e-cigarette. In contrast, alteration of respiratory function is observed in high-power ECA-exposed mice with a different profile than with CS. Subchronic exposure to ECA might alter the respiratory function independently of the inflammatory response and in a different manner than CS.