Role of PM(2.5) in the development and progression of COPD and its mechanisms

BACKGROUND: A multitude of epidemiological studies have shown that ambient fine particulate matter 2.5 (diameter < 2.5um; PM(2.5)) 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 PM(2.5) in the development of COPD and associated mechanisms. METHODS: We firstly conducted a cross-sectional study in Chinese han population to observe PM(2.5) effects on COPD morbidity. Then, in vitro, we incubated human bronchial epithelial cells to different concentrations of PM(2.5) for 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 PM(2.5) for 48 weeks to study the influence of PM(2.5) exposure on lung function, pulmonary structure and inflammation. RESULTS: We found that the effect of PM(2.5) on COPD morbidity was associated with its levels and that PM(2.5) and cigarette smoke could have a synergistic impact on COPD development and progression. Both vitro and vivo studies demonstrated that PM(2.5) exposure could induce pulmonary inflammation, decrease lung function, and cause emphysematous changes. Furthermore, PM(2.5) could markedly aggravated cigarette smoke-induced changes. CONCLUSIONS: In short, we found that prolonged chronic exposure to PM(2.5) resulted in decreased lung function, emphysematous lesions and airway inflammation. Most importantly, long-term PM(2.5) exposure exacerbateed cigarette smoke-induced changes in COPD.