肺
肺毒性
芯片上器官
微粒
细胞凋亡
医学
病理
免疫学
细胞生物学
药理学
化学
生物
材料科学
纳米技术
内科学
微流控
有机化学
生物化学
作者
Cong Xu,Min Zhang,Wenwen Chen,Lei Jiang,Chunying Chen,Jianhua Qin
出处
期刊:ACS Biomaterials Science & Engineering
[American Chemical Society]
日期:2020-03-24
卷期号:6 (5): 3081-3090
被引量:55
标识
DOI:10.1021/acsbiomaterials.0c00221
摘要
Airborne particulate matters have posed significant risk to human health worldwide. Fine particulate matters (PM2.5, aerodynamic diameter <2.5 μm) are associated with increased morbidity and mortality attributed to pulmonary diseases. An advanced in vitro model would benefit the assessment of PM2.5 induced pulmonary injuries and drug development. In this work, we present a PM2.5 exposure model to evaluate the pulmonary risk of fine particulate matter exposure in an organotypic manner with the help of 3D human lung-on-a-chip. By compartmentalized co-culturing of human endothelial cells, epithelial cells, and extra cellular matrix, our lung-on-a-chip recapitulated the structural features of the alveolar–blood barrier, which is pivotal for exogenous hazard toxicity evaluation. PM2.5 was applied to the channel lined with lung epithelial cells to model the pulmonary exposure of fine particulate matter. The results indicated acute high dose PM2.5 exposure would lead to various malfunctions of the alveolar–capillary barrier, including adheren junction disruption, increased ROS generation, apoptosis, inflammatory biofactor expression in epithelial cells and endothelial cells, elevated permeability, and monocyte attachments. Collectively, our lung-on-a-chip model provides a simple platform to investigate the complex responses after PM2.5 exposure in a physiologically relevant level, which could be of great potential in environmental risk assessment and therapeutic treatment development.
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