Liao Shi-Xia, Ding Ting, Rao Xi-Min, Sun De-Sheng, Sun Peng-Peng, Wang Ya-Jun, Fu Dan-Dan, Liu Xiao-Li, Ou-Yang Yao
Department of Respiratory Medicine, Affiliated Hospital of Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China.
Department of Osteopathy, Affiliated Hospital of Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China.
Mol Med Rep. 2015 Jan;11(1):219-25. doi: 10.3892/mmr.2014.2759. Epub 2014 Oct 23.
The aim of the present study was to characterize and quantify the numbers and expression levels of cells markers associated with dendritic cell (DC) maturation in small airways in current smokers and non-smokers with or without chronic obstructive pulmonary disease (COPD). Lung tissues from the following 32 patients were obtained during resection for lung cancer: Eight smokers with COPD, eight non-smokers with COPD, eight current smokers without COPD and eight non-smokers without COPD, serving as a control. The tissue sections were immunostained for cluster of differentiation (CD)83+ and CD1a+ to delineate mature and immature DCs, and chemokine receptor type 7 (CCR7+) to detect DC migratory ability. Myeloid DCs were collected from the lung tissues, and subsequently the CD83+ and CCR7+ expression levels in the lung myeloid DCs were detected using flow cytometry. The expression levels of CD83+, CD1a+ and CCR7+ mRNA in total lung RNA were evaluated by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Evident chronic bronchitis and emphysema pathological changes were observed in the lung tissues of patients with COPD. The results revealed that the numbers of CD83+ and CCR7+ DCs were reduced but the numbers of CD1a+ DCs were significantly increased in the COPD group as compared with the control group (P<0.05, respectively). Using RT-qPCR, the expression levels of CCR7+ and CD83+ mRNA were found to be reduced in the smokers with COPD as compared with the non-smokers without COPD group (P<0.05, respectively). Excessive local adaptive immune responses are key elements in the pathogenesis of COPD. Cigarette smoke may stimulate immune responses by impairing the homing of airway DCs to the lymph nodes and reduce the migratory potential of DCs. The present study revealed that COPD is associated with reduced numbers of mature CD83+ DCs and lower CCR7+ expression levels in small airways.
本研究的目的是对患有或未患有慢性阻塞性肺疾病（COPD）的当前吸烟者和非吸烟者小气道中与树突状细胞（DC）成熟相关的细胞标志物的数量和表达水平进行表征和量化。在肺癌切除术中获取了以下32例患者的肺组织：8例患有COPD的吸烟者、8例患有COPD的非吸烟者、8例无COPD的当前吸烟者和8例无COPD的非吸烟者，作为对照。对组织切片进行免疫染色，以检测分化簇（CD）83+和CD1a+，以描绘成熟和未成熟的DC，并检测趋化因子受体7型（CCR7+）以检测DC的迁移能力。从肺组织中收集髓样DC，随后使用流式细胞术检测肺髓样DC中CD83+和CCR7+的表达水平。通过逆转录定量聚合酶链反应（RT-qPCR）评估总肺RNA中CD83+、CD1a+和CCR7+ mRNA的表达水平。在COPD患者的肺组织中观察到明显的慢性支气管炎和肺气肿病理变化。结果显示，与对照组相比，COPD组中CD83+和CCR7+ DC的数量减少，但CD1a+ DC的数量显著增加（P分别<0.05）。使用RT-qPCR发现，与无COPD的非吸烟者组相比，患有COPD的吸烟者中CCR7+和CD83+ mRNA的表达水平降低（P分别<0.05）。过度的局部适应性免疫反应是COPD发病机制中的关键因素。香烟烟雾可能通过损害气道DC向淋巴结的归巢来刺激免疫反应，并降低DC的迁移潜力。本研究表明，COPD与小气道中成熟CD83+ DC数量减少和CCR7+表达水平降低有关。
