Department of Immunology, School of Basic Medical Sciences, Capital Medical University.
Department of Pulmonary and Critical Care Medicine, Center of Respiratory Medicine, China-Japan Friendship Hospital; National Center for Respiratory Medicine.
J Vis Exp. 2024 Jul 12(209). doi: 10.3791/67057.
Chronic obstructive pulmonary disease (COPD) is largely attributed to tobacco smoke exposure. Investigating how airway epithelial cells functionally adapt to tobacco smoke is crucial for understanding the pathogenesis of COPD. The present study was to set up an in vitro model using primary murine airway epithelial cells to mimic the real-life impact of tobacco smoke. Unlike established cell lines, primary cells retain more in vivo-like properties, including growth patterns, aging, and differentiation. These cells exhibit a sensitive inflammatory response and efficient differentiation, thus closely representing physiological conditions. In this model, primary murine airway epithelial cells were cultured for 28 days under an air-liquid interface with an optimal concentration of cigarette smoke extract (CSE), which led to the transformation of a monolayer of undifferentiated cells into a pseudostratified columnar epithelium, indicative of CSE acclimation. Comprehensive multi-omics analyses were then applied to elucidate the mechanisms by which CSE influences the differentiation of basal airway cells. These insights provide a deeper understanding of the cellular processes underpinning COPD progression in response to tobacco smoke exposure.
慢性阻塞性肺疾病（COPD）主要归因于烟草烟雾暴露。研究气道上皮细胞如何适应烟草烟雾对于理解 COPD 的发病机制至关重要。本研究通过使用原代鼠气道上皮细胞建立了一种体外模型，以模拟烟草烟雾的实际影响。与已建立的细胞系不同，原代细胞保留了更多类似体内的特性，包括生长模式、衰老和分化。这些细胞表现出敏感的炎症反应和有效的分化，因此更能代表生理条件。在该模型中，原代鼠气道上皮细胞在气液界面下培养 28 天，使用最佳浓度的香烟烟雾提取物（CSE），导致未分化细胞单层转化为假复层柱状上皮，表明 CSE 适应。然后应用综合多组学分析来阐明 CSE 影响基底气道细胞分化的机制。这些发现为理解烟草烟雾暴露引起的 COPD 进展中细胞过程提供了更深入的认识。
