Role of PM2.5 in the development and progression of COPD and its mechanisms
Role of PM2.5 in the development and progression of COPD and its mechanisms
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PM2.5在COPD发生、进展中的作用及其机制
DOI：
10.1186/s12931-019-1081-3
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发表时间：
2019-06-13
影响因子：
5.8
通讯作者：
Xie, Jungang
中科院分区：
文献类型：
--
作者：
Zhao, Junling;Li, Miao;Xie, Jungang
背景：大量流行病学研究表明，大气细颗粒物2.5（直径< 2.5um; PM2.5）与慢性阻塞性肺疾病（COPD）发病率和死亡率增加有关。然而，潜在的相关机制尚未阐明。本研究旨在探讨PM2.5在COPD发病中的作用及其相关机制。方法：采用横断面研究方法，在中国汉族人群中观察PM2.5对COPD发病的影响。然后，在体外，我们将人支气管上皮细胞与不同浓度的PM2.5孵育24小时。ELISA法检测IL-6、IL-8的表达水平，免疫印迹法检测MMPs、TGF-β1、FN和胶原的表达水平。在体内，我们将C57 BL/6小鼠长期暴露于PM2.5中，观察其对肺功能、肺结构和炎症的影响。结果：PM2.5对COPD发病的影响与其浓度有关，PM2.5和香烟烟雾对COPD的发生和发展有协同作用。体外和体内研究表明，PM2.5暴露可诱导肺部炎症，降低肺功能，并导致肺气肿的变化。结论：总之，我们发现长期慢性暴露于PM2.5可导致肺功能下降、肺气肿和气道炎症。最重要的是，长期PM2.5暴露加剧了吸烟引起的COPD变化。
Background:A multitude of epidemiological studies have shown that ambient fine particulate matter 2.5 (diameter < 2.5um; PM2.5) was associated with increased morbidity and mortality of chronic obstructive pulmonary disease (COPD). However, the underlying associated mechanisms have not yet been elucidated. We conducted this study to investigate the role of PM2.5in the development of COPD and associated mechanisms.Methods:We firstly conducted a cross-sectional study in Chinese han population to observe PM2.5effects on COPD morbidity. Then, in vitro, we incubated human bronchial epithelial cells to different concentrations of PM2.5for 24 h. The expression levels of IL-6 and IL-8 were detected by ELISA and the levels of MMPs, TGF-β1, fibronectin and collagen was determined by immunoblotting. In vivo, we subjected C57BL/6 mice to chronic prolonged exposure to PM2.5for 48 weeks to study the influence of PM2.5exposure on lung function, pulmonary structure and inflammation.Results:We found that the effect of PM2.5on COPD morbidity was associated with its levels and that PM2.5and cigarette smoke could have a synergistic impact on COPD development and progression. Both vitro and vivo studies demonstrated that PM2.5exposure could induce pulmonary inflammation, decrease lung function, and cause emphysematous changes. Furthermore, PM2.5could markedly aggravated cigarette smoke-induced changes.Conclusions:In short, we found that prolonged chronic exposure to PM2.5resulted in decreased lung function, emphysematous lesions and airway inflammation. Most importantly, long-term PM2.5exposure exacerbateed cigarette smoke-induced changes in COPD.