慢性阻塞性肺疾病诱导痰巨噬细胞Toll样受体-2表达及其意义

目的:探讨Toll样受体-2(TLR-2)在慢性阻塞性肺疾病(COPD)诱导痰巨噬细胞上的表达及其与气道炎症的关系。方法:20例COPD急性发作期(AECOPD)、16例COPD稳定期患者、年龄相当的正常人、支气管肺炎患者及健肺支气管肺泡灌洗者各10例纳入本研究。3%-5%氯化钠注射液进行痰液诱导,瑞氏染色行痰细胞分类计数,人淋巴细胞分离液行诱导痰单个核细胞分离。荧光物标记的抗人Toll样受体-2及CD14抗体行巨噬细胞双标,用流式细胞仪检测巨噬细胞平均荧光强度(rMFI)。结果:AECOPD、COPD稳定期、肺炎组诱导痰细胞总数、巨噬细胞及中性粒细胞数均显著高于正常对照组(P<0.01),肺炎组治疗后中性粒细胞数显著低于COPD稳定期组(P<0.01)。正常对照组及肺炎组疗前巨噬细胞TLR-2表达水平分别显著高于COPD稳定期、AECOPD治疗前后(P<0.01),肺炎组疗后则接近正常(P>0.05)。COPD稳定期、AECOPD巨噬细胞TLR-2表达水平与气道中性粒细胞数呈显著正相关(r=0.572,0.892,0.649,P<0.05或0.01)。结论:COPD诱导痰巨噬细胞TLR-2表达水平较正常人低下,这与COPD慢性气道炎症的形成密切相关。

Expression of Toll-Like Receptor 2 on Macrophages of Induced Sputum in Chronic Obstructive Pulmonary Disease

Objective: To explore the expression of Toll-like receptor 2 on macrophages of induced sputum in chronic obstructive pulmonary disease (COPD). Methods: Twenty patients with acute exacerbation of COPD(AECOPD), 16 patients with stable COPD, and 10 age-matched normal people and 10 bronchial pneumonia patients by bronchial-alveolar lavage were enrolled in the study. Induced sputum were collected by inhalation of 3%-5% sodium chloride. Cell numbers and differentials in sputum cell suspension were counted with Wright's stain. Mononuclear cells in induced sputum were separated by Ficoll-Hypaque. Macrophages of induced sputum were labelled by FITC-anti Toll-Like receptor 2(TCR-2) antibody and PE anti CD14 antibody, and flow cytometry were used to analyze relative mean fluorescence intensity(rMFI) of labelled macrophages. Results: The number of total sputum cells, macrophages and neutrophils in stable COPD, AECOPD and pneumonia group were significantly higher than those in normal group (P<0.01). In pneumonia group neutrophils counts were significantly less than in stable COPD group (P<0.01) after treatment. The level of TLR-2 expression in normal group was not different from that in bronchial-alveolar lavage (P>0.05), but was significantly higher than in stable COPD (P<0.01). In AECOPD, TLR-2 level was significantly higher than in stable COPD (P<0.01) before treatment and kept at relative higher level after treatment (P<0.01), but was significantly lower than in pneumonia group (P<0.01), which decreased to normal after treatment (P>0.05). The level of TLR-2 expression in stable COPD, AECOPD (before and after treatment) or pneumonia group was significantly positively correlated with neutrophils (r=0.572, 0.892, 0.649 and 0.788 respectively, all P<0.05 or 0.01). Conclusion: TLR-2 expression decreases on macrophages of induced sputum in COPD, which might result in persistent airway inflammation.