Wawryk-Gawda Ewelina, Zarobkiewicz Michał K, Wolanin-Stachyra Marta, Opoka-Winiarska Violetta
Department of Paediatric Pulmonology and Rheumatology, Medical University of Lublin, Lublin, Poland.
Department of Clinical Immunology, Medical University of Lublin, Lublin, Poland.
Front Immunol. 2025 Mar 21;16:1525166. doi: 10.3389/fimmu.2025.1525166. eCollection 2025.
Electronic cigarettes (e-cigarettes) were introduced two decades ago as a safer alternative to traditional cigarettes, aiming to assist in smoking cessation. However, the global use of e-cigarettes has surged, with the highest prevalence among adolescents and young adults. Despite their popularity, the safety of e-cigarettes remains controversial, with emerging evidence linking their use to various health risks, including cardiovascular issues, respiratory diseases, and a condition known as e-cigarette or vaping use-associated lung injury (EVALI). In this study, we investigated the inflammatory response in rats exposed to e-cigarette vapor compared to traditional cigarette smoke. We measured the serum concentrations of inflammatory markers such as IL-10, IFN-γ, IL-5, IL-2, TNF-α, GM-CS, IL-4, IL-9, IL-17F, IL-17A, IL-13, and IL-22 in the serum of rats subjected to 6 weeks of exposure. We assessed the activation of , , and genes and the expression of CXCL2 in lung tissues. Our results revealed a significant increase in proinflammatory cytokines, particularly in the vapor-exposed group. We did not observe any statistically significant difference in the activation levels of , , and between the groups of rats, but we noted the predictable correlations between IL-22 and IL-2, IL-6 and IL-2, IL-9 and IL-2, IL-6 and IL-9, IL-22 and IL-17F, IL-6 and IL-17F, IL-6 and IL-5, IL-2 and IL-17F, IL-13 and IL-4, and IL-5 and IL-4. In IHC staining, we observed a higher number of CLCX2-positive cells in the lung tissues in groups 2 and 3 compared to the control group. Interestingly, after a 2-week cessation period, inflammatory markers largely normalized, except for IL-17F and IL-13, which remained elevated in the cigarette smoke-exposed group. Our results suggest that while e-cigarette use may trigger a potent inflammatory response, the effects may be reversible upon cessation, albeit with some cytokines persisting longer in traditional cigarette users. Although the immune response has normalized, the increased tendency toward lung fibrosis may lead to permanent structural changes. Further research is needed to fully elucidate the clinical implications of these findings and assist in implementing legal regulations regarding the availability of e-cigarettes in the market.
电子烟于二十年前问世，作为传统香烟的一种更安全替代品，旨在帮助戒烟。然而，全球电子烟的使用量激增，在青少年和年轻人中患病率最高。尽管电子烟很受欢迎，但其安全性仍存在争议，越来越多的证据表明使用电子烟会带来各种健康风险，包括心血管问题、呼吸系统疾病以及一种名为电子烟或雾化产品使用相关肺损伤（EVALI）的病症。在本研究中，我们调查了与传统香烟烟雾相比，暴露于电子烟烟雾中的大鼠的炎症反应。我们测量了暴露6周的大鼠血清中炎症标志物如IL-10、IFN-γ、IL-5、IL-2、TNF-α、GM-CS、IL-4、IL-9、IL-17F、IL-17A、IL-13和IL-22的血清浓度。我们评估了 、 和 基因的激活情况以及肺组织中CXCL2的表达。我们的结果显示促炎细胞因子显著增加，尤其是在暴露于电子烟烟雾的组中。我们未观察到两组大鼠之间 、 和 的激活水平有任何统计学上的显著差异，但我们注意到IL-22与IL-2、IL-6与IL-2、IL-9与IL-2、IL-6与IL-9、IL-22与IL-17F、IL-6与IL-17F、IL-6与IL-5、IL-2与IL-17F、IL-13与IL-4以及IL-5与IL-4之间存在可预测的相关性。在免疫组化染色中，我们观察到与对照组相比，第2组和第3组肺组织中CLCX2阳性细胞数量更多。有趣的是，在2周的戒断期后，除了IL-17F和IL-13在暴露于香烟烟雾的组中仍保持升高外，炎症标志物在很大程度上恢复正常。我们的结果表明，虽然使用电子烟可能引发强烈的炎症反应，但戒断后这种影响可能是可逆的，尽管某些细胞因子在传统香烟使用者中持续时间更长。虽然免疫反应已恢复正常，但肺纤维化增加的趋势可能导致永久性结构变化。需要进一步研究以充分阐明这些发现的临床意义，并协助实施有关电子烟在市场上可获得性的法律法规。
