Integrative characterization of fine particulate matter-induced chronic obstructive pulmonary disease in mice
Integrative characterization of fine particulate matter-induced chronic obstructive pulmonary disease in mice
复制标题
细颗粒物诱发的小鼠慢性阻塞性肺疾病的综合特征。
DOI：
10.1016/j.scitotenv.2019.135687
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发表时间：
2020-03-01
影响因子：
9.8
通讯作者：
Tian, Lin
中科院分区：
文献类型：
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作者：
Li, Qiuyue;Sun, Jingping;Tian, Lin
环境细颗粒物（PM2.5）对公众健康的影响是全世界关注的问题。流行病学证据表明，PM2.5引发的炎症级联反应和肺组织损伤是慢性阻塞性肺病（COPD）的重要原因。然而，大多数慢性阻塞性肺病的实验室研究都集中在香烟烟雾暴露或香烟烟雾和 PM2.5 联合暴露的动物模型上。此外，使用单一方法来评估COPD的发展，缺乏完整性。在这项研究中，我们使用综合功能、形态学和生化技术以及仅暴露于 PM2.5 3 个月的小鼠模型来研究肺部病理生理学变化。该模型中的肺气肿通过重建的三维显微 CT 图像得到证实。典型的组织病理学迹象是暴露后2个月时中性粒细胞/巨噬细胞浸润和积聚以及3个月时肺气肿不张。呼吸机械参数证实PM2.5导致呼吸功能下降。 PM2.5 还会引发肺部复杂的细胞因子谱变化，并伴有典型的炎症相关组织破坏。这项研究表明，长期接触 PM2.5 会损害肺功能，引发肺气肿病变，并诱发肺部炎症和气道壁重塑。最重要的是，长期单独暴露于 PM2.5 会导致小鼠出现慢性阻塞性肺病。这些结果增进了对 PM2.5 诱发 COPD 的机制和介质的理解。 (C) 2018 Elsevier B.V. 保留所有权利。
The impacts of ambient fine particulate matter (PM2.5) on public health are a worldwide concern. Epidemiological evidence has shown that PM2.5-triggered inflammatory cascades and lung tissue damage are important causes of chronic obstructive pulmonary disease (COPD). However, most laboratory studies of COPD have focused on animal models of cigarette smoke exposure or combined exposure to cigarette smoke and PM2.5. Furthermore, a single method is used to evaluate the development of COPD without integrality. In this study, we investigated pulmonary pathophysiological alterations using integrated functional, morphological, and biochemical techniques and a mouse model exposed to PM2.5 alone for 3 months. Emphysema in this model was confirmed by reconstructed three-dimensional micro-CT images. Typical histopathological signs were neutrophil/macrophage infiltration and accumulation at 2 months after exposure and emphysemalatelectasis at 3 months. Respiratory mechanical parameters confirmed that PM2.5 caused a decline in respiratory function. PM2.5 also triggered complex cytokine profile changes in the lungs with characteristic inflammation-related tissue destruction. This study showed that chronic PM2.5 exposure impaired lung function, triggered emphysematous lesions, and induced pulmonary inflammation and airway wall remodeling. Most importantly, prolonged exposure to PM2.5 alone caused COPD in mice. These results improve the understanding of the mechanisms and mediators underlying PM2.5-induced COPD. (C) 2018 Elsevier B.V. All rights reserved.