Quantitative differentiation of dendritic cells in lung tissues of smokers with and without chronic obstructive pulmonary disease

Background Chronic obstructive pulmonary disease (COPD) is thought to be an inflammatory immune response disease. In most cases, the disease is caused by cigarette smoke, but it has been demonstrated that only 10% to 20% of smokers will definitely suffer from COPD. Dendritic cells (DCs) are considered to be the promoter of immune responses. However, the underlying mechanisms involved are still unrevealed. In this study, we aimed to investigate the quantitative differentiation of pulmonary DC in smokers with or without COPD to explore the possible role of DCs in smokers suffering COPD. Methods Peripheral lung specimens from non-smokers without airflow obstruction (control group, n=7), smokers without airflow obstruction (smoker group, n=7) and patients with COPD (COPD group, n=7) were investigated to detect the quantity of S-100 and CD1a positive cells by immunohistochemical or immunofluorescent assay. Results In smokers with COPD, the number of S-100(+) DCs was higher than in the controls and smokers without COPD (P <0.01 and P <0.05) and there was a higher number of S-100+ DCs in smokers with COPD than in smokers without COPD, but without a significant difference (P >0.05). An inverse correlation was found between the number of DCs and forced expiratory volume in the first second (FEV1)% pred (r=-0.75, P <0.05), which was also found between the number of DCs and FEV1/forced vital capacity (FVC) (r=-0.72, P <0.05). The mean number of CD1a(+)DCs, increased from non-smokers to non-COPD smokers to CORD patients, with significant differences between each group (P <0.01). Conclusions The quantity of DCs significantly increased in smokers with COPD compared with non-smokers or smokers without COPD. The results suggest that DCs may play an important role in the pathogenesis of smoking-induced COPD, and the upregulation of DCs may be a potential maker to identify the smokers who have more liability to suffer from COPD. Chin Med J 2010;123(12):1500-1504