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

Abstract 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. Topic Categories Immune Mechanisms of Human Disease (HUM)