Wang Shao-gang, Bai Jian, Xi Qi-lin, Hu Dong-liang, Liu Ji-hong, Ye Zhang-qun
Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Zhonghua Yi Xue Za Zhi. 2008 Nov 4;88(40):2838-41.
To explore the role of CD4+CD25+ regulatory T cells in the pathogenesis of chronic abacterial prostatitis/chronic pelvic pain syndrome (CAP/CPPS).
Peripheral blood samples were collected from 45 CAP/CPPS patients and 18 healthy age-matched male persons. Peripheral blood mononuclear cells (PBMCs) were isolated. The percentages of CD4+CD25+ and CD4+CD25high regulatory T cells were detected by flow cytometry. PCR was used to examine the mRNA expression of Foxp3, a transcription factor expressed in the CD4+CD25+ cells. ELISA was used to examine the plasma level of tumor growth factor (TGF)-beta1.
There were no significant differences in the percentages of peripheral blood CD4+CD25+ and CD4+CD25highT cells between the CAP/CPPS patients and normal control group (both P>0.05). The Foxp3 mRNA in the PBMCs of the CAP/CPPS IIIA and CAP/CPPS IIIB patients were (0.69+/-0.23) and (0.44+/-0.18) respectively, both significantly lower than that of the control group [(1.37+/-0.19), P<0.05]. The serum TGF-beta1 levels of the CAP/CPPS IIIA and CAP/CPPS IIIB patients were (18.09+/-10.45) pg/ml and (14.06+/-6.22) pg/ml respectively, both significantly lower than that of the control group [(27.01+/-13.29) pg/ml, both P<0.05].
Not the number of peripheral blood CD4+CD25+ regulatory T cells, but its defective function participates in the pathogenesis of CAP/CPPS. The Foxp3 gene and TGF-beta1 play important roles in the process of pathogenesis of CAP/CPPS too.
探讨CD4+CD25+调节性T细胞在慢性非细菌性前列腺炎/慢性盆腔疼痛综合征(CAP/CPPS)发病机制中的作用。
收集45例CAP/CPPS患者及18例年龄匹配的健康男性外周血样本。分离外周血单个核细胞(PBMCs)。采用流式细胞术检测CD4+CD25+及CD4+CD25high调节性T细胞的百分比。采用聚合酶链反应(PCR)检测CD4+CD25+细胞中表达的转录因子Foxp3的mRNA表达。采用酶联免疫吸附测定(ELISA)检测血浆中肿瘤生长因子(TGF)-β1水平。
CAP/CPPS患者与正常对照组外周血CD4+CD25+及CD4+CD25highT细胞百分比差异均无统计学意义(均P>0.05)。CAP/CPPS IIIA组和CAP/CPPS IIIB组患者PBMCs中Foxp3 mRNA分别为(0.69±0.23)和(0.44±0.18),均显著低于对照组[(1.37±0.19),P<0.05]。CAP/CPPS IIIA组和CAP/CPPS IIIB组患者血清TGF-β1水平分别为(18.09±10.45)pg/ml和(14.06±6.22)pg/ml,均显著低于对照组[(27.01±13.29)pg/ml,均P<0.05]。
参与CAP/CPPS发病机制的不是外周血CD4+CD25+调节性T细胞的数量,而是其功能缺陷。Foxp3基因和TGF-β1在CAP/CPPS发病机制中也起重要作用。