期刊
VIRCHOWS ARCHIV
卷 454, 期 3, 页码 273-281出版社
SPRINGER
DOI: 10.1007/s00428-009-0727-9
关键词
Adenosine; Adenosine receptors; COPD; Smoking cessation
类别
资金
- Groningen University Graduate School for Drug Exploration (GUIDE)
Our group has shown that 1-year smoking cessation persisted or increased airway inflammation in chronic obstructive pulmonary disease (COPD). We compared adenosine and adenosine receptor (AR) expression in COPD and asymptomatic smokers (AS) before and after 1-year smoking cessation. Sputum cytospins and bronchial biopsies of (ex)smoking COPD patients and AS were studied for A(1)R, A(2A)R, A(2B)R, and A(3)R expression. Adenosine and inflammatory mediators were measured in sputum supernatants. At baseline, COPD patients had lower levels of adenosine and higher levels of vascular endothelial growth factor in sputum than AS. Smoking cessation induced significantly different effects in COPD than in AS, i.e. an increase in percentages of A(3)R expressing neutrophils and A(1)R expressing macrophages in COPD as increase in adenosine and monocyte chemoattractant protein-1 levels in sputum. Adenosine-related effector mechanisms may contribute to the persistence and progression of airway inflammation in COPD following 1-year smoking cessation.
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