Exposure to Air Pollution Exacerbates Inflammation in Rats with Preexisting COPD
Exposure to Air Pollution Exacerbates Inflammation in Rats with Preexisting COPD
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暴露于空气污染会加剧患有慢性阻塞性肺病的老鼠的炎症
DOI：
10.1155/2020/4260204
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发表时间：
2020-05
影响因子：
4.6
通讯作者：
Li Jiansheng
中科院分区：
文献类型：
--
作者：
Wang Jing;Li Ya;Zhao Peng;Tian Yange;Liu Xuefang;He Huihui;Jia Rui;Oliver G. Brian;Li Jiansheng
空气动力学直径等于或小于2.5微米的颗粒物（PM2.5）与慢性阻塞性肺疾病（COPD）的发展有关。PM2.5加速COPD疾病进展的机制尚不清楚。在本研究中，我们旨在探讨PM2.5对COPD大鼠肺损伤的影响。通过重复吸入香烟烟雾和细菌感染8周，在大鼠模型中诱导人类慢性阻塞性肺病的主要特征。然后，从第9周到第16周，对部分COPD大鼠进行实时浓度大气PM2.5检测。测量肺功能、病理、炎症细胞因子、氧化应激、粘液和胶原蛋白的产生。正如预期的那样，COPD大鼠出现了肺气肿、炎症和肺功能恶化。PM2.5暴露导致肺功能下降和组织病理学改变更大，表现为肺组织中黏液蛋白（mucc） 5ac、MUC5b、I型胶原蛋白、III型胶原蛋白以及促纤维化细胞因子α-平滑肌肌动蛋白（SMA）、转化生长因子- (TGF-) β1升高。PM2.5还会加重炎症，增加支气管肺泡灌洗液（BALF）中的中性粒细胞和嗜酸性粒细胞以及白细胞介素- (IL-) 1β、粒细胞-巨噬细胞集落刺激因子（GM-CSF）和IL-4等细胞因子。可能的机制是通过氧化应激，因为抗氧化剂水平下降，而氧化剂增加，这表明氧化-抗氧化平衡发生了有害的变化。综上所述，PM2.5暴露可通过损害肺功能和加重肺损伤来促进COPD的发展，其潜在机制可能与炎症反应和氧化应激有关。
Particulate matter with an aerodynamic diameter equal or less than 2.5 micrometers (PM2.5) is associated with the development of chronic obstructive pulmonary disease (COPD). The mechanisms by which PM2.5 accelerates disease progression in COPD are poorly understood. In this study, we aimed to investigate the effect of PM2.5 on lung injury in rats with hallmark features of COPD. Cardinal features of human COPD were induced in a rat model by repeated cigarette smoke inhalation and bacterial infection for 8 weeks. Then, from week 9 to week 16, some of these rats with COPD were subjected to real-time concentrated atmospheric PM2.5. Lung function, pathology, inflammatory cytokines, oxidative stress, and mucus and collagen production were measured. As expected, the COPD rats had developed emphysema, inflammation, and deterioration in lung function. PM2.5 exposure resulted in greater lung function decline and histopathological changes, as reflected by increased Mucin (MUC) 5ac, MUC5b, Collagen I, Collagen III, and the profibrotic cytokine α-smooth muscle-actin (SMA), transforming growth factor- (TGF-) β1 in lung tissues. PM2.5 also aggravated inflammation, increasing neutrophils and eosinophils in bronchoalveolar lavage fluid (BALF) and cytokines including Interleukin- (IL-) 1β, granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-4. The likely mechanism is through oxidative stress as antioxidants levels were decreased, whereas oxidants were increased, indicating a detrimental shift in the oxidant-antioxidant balance. Altogether, these results suggest that PM2.5 exposure could promote the development of COPD by impairing lung function and exacerbating pulmonary injury, and the potential mechanisms are related to inflammatory response and oxidative stress.
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DOI：
10.1164/rccm.200811-1757st
发表时间：
2010-09-01
影响因子：
24.7
作者：
Eisner, Mark D.;Anthonisen, Nicholas;Balmes, John R.
通讯作者：
Balmes, John R.
DOI：
10.1056/nejmra0910061
发表时间：
2010-12-02
期刊：
The New England journal of medicine
影响因子：
--
作者：
Fahy JV;Dickey BF
通讯作者：
Dickey BF
机动粒子，组成和肺部疾病。
影响因子：
7.3
作者：
Falcon-Rodriguez CI;Osornio-Vargas AR;Sada-Ovalle I;Segura-Medina P
通讯作者：
Segura-Medina P
DOI：
10.1016/s0140-6736(18)32225-6
发表时间：
2018-11-10
期刊：
Lancet (London, England)
影响因子：
--
作者：
GBD 2017 Risk Factor Collaborators
通讯作者：
GBD 2017 Risk Factor Collaborators
影响因子：
158.5
作者：
HOGG, JC;MACKLEM, PT;THURLBECK, WM
通讯作者：
THURLBECK, WM