Abstract
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.
Highlights
Chronic obstructive pulmonary disease (COPD) is an international health problem with a rising prevalence and mortality and is estimated to be the third commonest cause of death and the fifth leading cause of disability by 2020 [1, 2]
Our results demonstrated that PM2.5 exposure significantly impaired lung function and histology in COPD rats
This is the first study to evaluate the effect of PM2.5 on preexisting COPD in multiple aspects using a whole-body PM2.5 exposure system, which mimic the clinical situation in many countries with episodic increases in PM2.5 pollution
Summary
Chronic obstructive pulmonary disease (COPD) is an international health problem with a rising prevalence and mortality and is estimated to be the third commonest cause of death and the fifth leading cause of disability by 2020 [1, 2]. It is characterized by persistent airflow limitation and chronic airway inflammation typically caused and worsened by inhalation of noxious gases or particles [3]. Ambient PM2.5 has been recognized as a major detrimental risk factor for the development, progression, and exacerbation of COPD
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