The following is a summary of “E-cigarette vapor renders neutrophils dysfunctional due to filamentous actin accumulation,” published in the January 2024 issue of Allergy & Immunology by Jasper, et al.
Despite concerns about their long-term effects, the use of electronic cigarettes (e-cigarettes) continues to rise, particularly regarding the risk of developing lung diseases like chronic obstructive pulmonary disease (COPD). Neutrophils play a crucial role in COPD pathogenesis, with changes in their phenotype and function implicated in tissue damage. For a study, researchers sought to assess the impact of direct exposure to nicotine-containing and nicotine-free e-cigarette vapor on human neutrophil function and phenotype.
Neutrophils were isolated from the whole blood of self-reported nonsmoking, non-vaping healthy volunteers and exposed to 40 puffs of e-cigarette vapor generated from flavorless e-cigarette liquids with and without nicotine. Neutrophil functions, deformability, and phenotype were then assessed.
The study found that exposure to e-cigarette vapor altered neutrophil surface marker expression, notably reducing CD62L and CXCR2 expression in neutrophils treated with nicotine-containing vapor. Furthermore, neutrophil migration, phagocytosis, oxidative burst response, and neutrophil extracellular trap formation were all significantly reduced by e-cigarette vapor treatments, regardless of nicotine content. Additionally, e-cigarette vapor induced increased baseline polymerized filamentous actin levels in the cytoplasm compared to untreated controls.
In conclusion, exposure to high-power e-cigarette devices, even in the absence of nicotine, significantly reduced effector neutrophil functions and induced excessive filamentous actin polymerization. The findings underscored the potentially harmful effects of vaping on respiratory health and emphasized the need for further research to uncover the long-term health implications of e-cigarette use.
Reference: jacionline.org/article/S0091-6749(23)01107-7/fulltext