Department of Cell Biology and Physiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Nicotine Tob Res. 2022 Feb 14;24(3):395-399. doi: 10.1093/ntr/ntab186.
Alveolar macrophages (AMs) are lung-resident immune cells that phagocytose inhaled particles and pathogens, and help coordinate the lung's immune response to infection. Little is known about the impact of chronic e-cigarette use (ie, vaping) on this important pulmonary cell type. Thus, we determined the effect of vaping on AM phenotype and gene expression.
We recruited never-smokers, smokers, and e-cigarette users (vapers) and performed research bronchoscopies to isolate AMs from bronchoalveolar lavage fluid samples and epithelial cells from bronchial brushings. We then performed morphological analyses and used the Nanostring platform to look for changes in gene expression.
AMs obtained from smokers and vapers were phenotypically distinct from those obtained from nonsmokers, and from each other. Immunocytochemistry revealed that vapers AMs had significantly elevated inducible nitric oxide synthase (M1) expression and significantly reduced CD301a (M2) expression compared with nonsmokers or smokers. Vapers' AMs and bronchial epithelia exhibited unique changes in gene expression compared with nonsmokers or smokers. Moreover, vapers' AMs were the most affected of all groups and had 124 genes uniquely downregulated. Gene ontology analysis revealed that vapers and smokers had opposing changes in biological processes.
These data indicate that vaping causes unique changes to AMs and bronchial epithelia compared with nonsmokers and smokers which may impact pulmonary host defense.
These data indicate that normal "healthy" vapers have altered AMs and may be at risk of developing abnormal immune responses to inflammatory stimuli.
肺泡巨噬细胞（AMs）是肺驻留免疫细胞，可吞噬吸入的颗粒和病原体，并有助于协调肺部对感染的免疫反应。对于慢性电子烟使用（即蒸气）对这种重要的肺细胞类型的影响知之甚少。因此，我们确定了蒸气对 AM 表型和基因表达的影响。
我们招募了从不吸烟者、吸烟者和电子烟使用者（蒸气者），并进行了研究性支气管镜检查，以从支气管肺泡灌洗液样本和支气管刷取物中分离 AM。然后，我们进行了形态分析，并使用 Nanostring 平台寻找基因表达的变化。
与从不吸烟者或吸烟者相比，吸烟者和蒸气者获得的 AM 在表型上明显不同，而且彼此之间也不同。免疫细胞化学显示，与从不吸烟者或吸烟者相比，蒸气者的 AM 诱导型一氧化氮合酶（M1）表达明显升高，CD301a（M2）表达明显降低。与从不吸烟者或吸烟者相比，蒸气者的 AM 和支气管上皮细胞表现出独特的基因表达变化。此外，与所有其他组相比，蒸气者的 AM 受影响最大，有 124 个基因特异性下调。基因本体分析表明，蒸气者和吸烟者的生物学过程发生了相反的变化。
这些数据表明，与从不吸烟者和吸烟者相比，蒸气会引起 AM 和支气管上皮细胞的独特变化，这可能会影响肺部宿主防御。
这些数据表明，正常的“健康”蒸气者的 AM 发生了改变，并且可能有发展出对炎症刺激异常免疫反应的风险。
