期刊
SCIENCE OF THE TOTAL ENVIRONMENT
卷 706, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.scitotenv.2019.135687
关键词
PM2.5; COPD; Emphysema
资金
- National Natural Science Foundation of China [91643114, 81602832]
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据