BRIEF RESEARCH REPORT article
Front. Immunol.
Sec. Inflammation
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1665936
This article is part of the Research TopicRole of Extracellular Vesicles in InflammationView all 8 articles
E-Cigarette Vapor Amplifies Neutrophilic Inflammation and Proteolytic EVs in Response to LPS
Provisionally accepted
Lawrence W RasmussenDakota C FinleyJulian B SmithAaron S Noa
Amit Gaggar
J. Edwin Blalock
Matthew Cameron Madison*- The University of Alabama at Birmingham, Birmingham, United States
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Background: While e-cigarette use (vaping) has increased in the last decade, its effects on airway inflammation and extracellular vesicle (EV) biology remain unclear. This study examined how long-term and acute vapor exposures influence lung immune responses, neutrophilic inflammation, and EV-associated proteolytic activity.Methods: Mice were exposed daily to vapor from commercial e-cigarettes or room air for up to 12 weeks. After exposure, we assessed immune cell recruitment, alveolar damage, and EV populations in the airways. To explore vapor-mediated effects on secondary lung injury, a lipopolysaccharide (LPS) challenge was administered after two weeks of vapor exposure. We then analyzed immune cell responses and isolated neutrophil-derived EVs (nEVs) for transfer into naïve mice to evaluate pathogenic potential.Results: Vapor exposure alone did not significantly alter immune cell infiltration, lung histology, or EV protease activity. However, mice pre-exposed to vapor and then challenged with LPS showed increased neutrophil infiltration, elevated neutrophil elastase activity in EVs, and greater alveolar damage. Furthermore, nEVs from these mice induced more severe emphysematous changes when transferred to unexposed mice.Conclusions: While e-cigarette vapor alone does not provoke marked airway inflammation or proteolytic EV release, it creates a primed immune state. This priming amplifies inflammatory and destructive responses to subsequent challenges. These findings suggest vaping may exacerbate lung damage when combined with infections or other environmental stressors, raising concerns about its role in worsening pulmonary disease.
Keywords: Neutrophil, elastase, Extracellular vesicle, e-Cigarette, vaping
Received: 14 Jul 2025; Accepted: 12 Aug 2025.
Copyright: © 2025 Rasmussen, Finley, Smith, Noa, Gaggar, Blalock and Madison. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Matthew Cameron Madison, The University of Alabama at Birmingham, Birmingham, United States
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.