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.

中文翻译：

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暴露于空气污染会加剧患有COPD的大鼠的炎症。

空气动力学直径等于或小于2.5微米（PM2.5）的颗粒物与慢性阻塞性肺疾病（COPD）的发展有关。人们对PM2.5促进COPD疾病进展的机制了解甚少。在这项研究中，我们旨在研究PM2.5对具有COPD标志性特征的大鼠肺损伤的影响。通过重复吸入烟气和细菌感染8周，在大鼠模型中诱导人COPD的基本特征。然后，从第9周到第16周，对其中一些患有COPD的大鼠进行实时浓缩的大气PM2.5监测。测量了肺功能，病理学，炎性细胞因子，氧化应激以及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。α-平滑肌肌动蛋白（SMA），肺组织中的转化生长因子-（TGF-）β1。PM2.5还加剧了炎症，增加了支气管肺泡灌洗液（BALF）和细胞因子（包括白介素-（IL-）1β，粒细胞-巨噬细胞集落刺激因子（GM-CSF）和IL-4）的嗜中性粒细胞和嗜酸性粒细胞。可能的机理是由于抗氧化剂水平降低而氧化剂增加而引起的氧化应激，表明氧化剂-抗氧化剂平衡的有害变化。总之，这些结果表明，PM2.5暴露可通过损害肺功能和加剧肺损伤来促进COPD的发展，其潜在机制与炎症反应和氧化应激有关。