Electronic cigarette (E-Cigarette) vapor amplifies inflammation and the pathogenic extracellular vesicle signature associated with LPS-driven lung injury 3771

Description Background E-cigarette use has surged as an alternative to traditional smoking, but the pulmonary effects of e-cigarette vapor remain poorly understood. Previous work has shown that bacterial components like lipopolysaccharide (LPS) trigger the generation of pathogenic, neutrophil-derived extracellular vesicles (EVs) expressing destructive proteases, such as neutrophil elastase (NE). This study aimed to determine whether e-cigarette vapor modulates the EV signature linked to LPS exposure. Methods Wild-type mice were pre-exposed to ambient air or e-cigarette vapor for 2 weeks. Mice then received intratracheal LPS treatment, and pulmonary inflammation and alveolar damage were assessed over time. Results Mice pre-exposed to e-cigarette vapor exhibited heightened inflammation and greater alveolar damage upon LPS treatment compared to air-exposed mice. The vapor-exposed, LPS-treated mice also had a more destructive EV signature with increased protease activity. When these EVs were transferred to naïve mice, they caused more severe lung damage compared to EVs from air-exposed LPS-treated mice. Conclusions E-cigarette vapor appears to enhance lung injury and inflammation, highlighting the need for further investigation into the mechanisms by which vapor may increase lung susceptibility to damage.