慢性阻塞性肺疾病患者外周血单个核细胞CXC趋化因子受体3表达的意义  

Study on mRNA expression of CXCR3 on peripheral blood mononuclear cells of patients with chronic obstrucitve pulmonary disease

作　　者：聂莉[1] 李婷[1] 刘淑华[1] 刘以鹏[1] 

机构地区：[1]武汉大学人民医院老年病科,430060

出　　处：《临床内科杂志》2012年第3期170-172,共3页Journal of Clinical Internal Medicine

基　　金：中央高校基本科研业务费专项资金青年教师资助项目（批准号：4101027）

摘　　要：目的探讨CXC趋化因子受体3（CXCR3）在慢性阻塞性肺疾病（COPD）发病机制中的作用及临床意义。方法选择COPD急性加重期、稳定期患者和对照组各30例，采用流式细胞术检测外周血单个核细胞中T细胞亚群CD8^＋T细胞和CD4T细胞数，实时荧光定量聚合酶链反应检测CXCR3、干扰素-γ（IFN-γ）、IL-4和干扰素-1诱导蛋白-10（CXCLIO）mRNA的表达。结果流式细胞术检测结果显示，COPD急性加重期患者PMBCs中CD8^＋T细胞数较COPD稳定期组及对照组明显增高（P〈0．05）；且COPD稳定期组较对照组明显升高（P〈0．05）。在mRNA水平，与COPD急性加重期组相比，COPD稳定期组和对照组PMBCs中CXCR3、CXCL10和IFN-γ的表达水平均明显降低（P〈0．05）。与对照组相比，COPD稳定期组PMBCs中CXCR3、CXCL10和IFN-1mRNA的表达水平显著上调（P〈0．05）。三组间IL-4mRNA的表达比较差异无统计学意义（P〉0．05）。结论CXCR3可通过募集CDsT细胞及促进IFN-γ和CXCL10等细胞因子的释放而启动COPD急性加重期的炎症级联反应。因此，CXCR3可作为治疗COPD肺部炎症的新目标。Objective To investigate the roles of CXCR3 in the pathogenesis of chronic obstructive pulmonary diseasea（COPD） and its clinical significance. Methods 30 patients with COPD during a- cute exacerbation （AECOPD）, 30 patients with COPD stable period, and 30 normal persons （control group） were chosen. Flow cytometry were used to mesure CD4 T cells and CDs T cells on the PBMCs. Expression of CXCR3, Interferon-γ（ IFN-γ ）, Interleukin 4 （ IL-4 ） and Interferon-γ induced protein-10 （CXCLIO） at mRNA levels were detected by real-time quantitative PCR. Results Flow cytometry indicated that CDs T cells on the PBMCs of the patients with AECOPD was significantly increased compared to the patients with COPD stable period and the control group（P 〈0.05）. While CDsT cells in the patients with COPD stable period was profoundly increased compared to the control group（ P 〈 0.05 ）. At the mRNA level, there were significantly higher levels of CXCR3, CXCL10 and IFN-γ on the PBMCs of the patients with AECOPD compared to the patients with COPD stable period and the control group （P 〈 0.05）. The expression of CXCR3, CXCL10 and IFN-＇y mRNA in the control group were significant lower than that in the patients with COPD stable period（P 〈 0.05 ）. In the IL-4 mRNA expression,there was no significant difference occurring between the three groups （P 〉 0.05 ）. Conclusion CXCR3 can triggers the inflammatory response cascade in AECOPD by promoting CD8^＋ T ceils recruitment and initiating IFN-γ and CXCL10 release. Therefore, CXCR3 may be a novel therapeutic target for COPD treatment.

关 键 词：慢性阻塞性肺疾病 CXC趋化因子受体3 外周血单个核细胞 

分 类 号：R563[医药卫生—呼吸系统]