E-cigarettes (eCig) are being considered as an alternative to quit cigarette smoking while their long-term effect on lung pathophysiology are unknown. Maternal eCig-vaping may be promoted and considered as a safer cigarette smoking-replacement during pregnancy thus needing further assessment. Using murine models of in utero vaping and allergic asthma with complementary in vitro experiments we tested whether maternal eCig vaping enhances features of allergic asthma in offspring. Female BALB/c mice were exposed to either eCig vapor (± nicotine) or room air. Female offspring from these mothers were subjected to an ovalbumin (OVA)-induced allergic asthma model. Lung function and airway inflammation was assessed. Tissues were histologically assessed with H&E, Periodic Acid-Schiff and Masson's trichrome. Mitochondrial homeostasis protein expression was measured using immunohistochemistry while human airway smooth muscle (ASM) and Beas-2B cells were used to further measure cellular function and mitochondrial respiration. Allergen-challenge in mice lead to significant increase in airway inflammation, development of airway hyperresponsiveness (AHR) and increase in mucus and airway wall thickening (hallmark features of allergic asthma). Allergic asthma features were significantly enhanced in offspring from eCig (+Nicotine)-exposed mothers and were mainly reliant upon Th2-dependent inflammation with complementary changes in mitochondrial homeostasis. Further, in vitro data demonstrated that eCig (±Nicotine)-exposure impaired airway cell homeostasis and perturbed mitochondrial function. Collectively, maternal eCig vaping enhanced and worsened features of allergic asthma and this could partly be attributed to aberrant mitochondrial function.

中文翻译：

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在子宫内接触含有尼古丁的电子烟会增加女性后代患过敏性哮喘的风险。


电子烟（eCig）被认为是戒烟的替代品，但其对肺部病理生理学的长期影响尚不清楚。母亲电子烟可能会被推广并被视为怀孕期间更安全的吸烟替代品，因此需要进一步评估。使用子宫内电子烟和过敏性哮喘的小鼠模型以及补充体外实验，我们测试了母亲电子烟是否会增强后代过敏性哮喘的特征。雌性 BALB/c 小鼠暴露于电子烟蒸汽（±尼古丁）或室内空气中。这些母亲的雌性后代接受了卵清蛋白（OVA）诱导的过敏性哮喘模型。评估肺功能和气道炎症。用 H&E、Periodic Acid-Schiff 和 Masson's trichrome 对组织进行组织学评估。使用免疫组织化学测量线粒体稳态蛋白表达，同时使用人气道平滑肌 (ASM) 和 Beas-2B 细胞进一步测量细胞功能和线粒体呼吸。小鼠的过敏原挑战会导致气道炎症显着增加、气道高反应性（AHR）的发展以及粘液和气道壁增厚（过敏性哮喘的标志特征）的增加。暴露于电子烟（+尼古丁）的母亲的后代的过敏性哮喘特征显着增强，并且主要依赖于 Th2 依赖性炎症以及线粒体稳态的互补变化。此外，体外数据表明，接触电子烟（±尼古丁）会损害气道细胞稳态并扰乱线粒体功能。总的来说，母亲吸电子烟会增强和恶化过敏性哮喘的特征，这可能部分归因于线粒体功能异常。