定量分析吸烟人群中伴或不伴慢性阻塞性肺疾病患者的肺部树突状细胞分化。

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

机构信息

Department of Respiratory Medicine, Tongji Hospital affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.

出版信息

Chin Med J (Engl). 2010 Jun;123(12):1500-4.

PMID:20819500

Abstract

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 (FEV(1))% pred (r = -0.75, P < 0.05), which was also found between the number of DCs and FEV(1)/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 COPD 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.

摘要

背景

慢性阻塞性肺疾病（COPD）被认为是一种炎症免疫反应性疾病。在大多数情况下，这种疾病是由香烟烟雾引起的，但已经证明，只有 10%到 20%的吸烟者肯定会患上 COPD。树突状细胞（DCs）被认为是免疫反应的促进者。然而，其潜在的机制仍未被揭示。在这项研究中，我们旨在研究吸烟者中肺 DC 的定量分化，以探索 DCs 在吸烟者患 COPD 中的可能作用。

方法

检测非吸烟无气流阻塞者（对照组，n=7）、吸烟无气流阻塞者（吸烟者组，n=7）和 COPD 患者（COPD 组，n=7）的外周肺标本，通过免疫组化或免疫荧光检测 S-100 和 CD1a 阳性细胞的数量。

结果

在 COPD 吸烟者中，S-100（+）DC 数量高于对照组和非 COPD 吸烟者（P<0.01 和 P<0.05），且 COPD 吸烟者中的 S-100（+）DC 数量高于非 COPD 吸烟者，但无显著性差异（P>0.05）。发现 DC 数量与第一秒用力呼气量（FEV（1））%预测值之间呈负相关（r=-0.75，P<0.05），与 FEV（1）/用力肺活量（FVC）之间也呈负相关（r=-0.72，P<0.05）。CD1a（+）DC 的平均数量从非吸烟者到非 COPD 吸烟者再到 COPD 患者逐渐增加，各组之间有显著差异（P<0.01）。