Role of PM _2.5 in the development and progression of COPD and its mechanisms

Abstract

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.