Role of CD4+ CDhigh25 regulatory T cells and relative cytokines on the pathogenesis of chronic abacterial pros-tatitis/chronic pelvic pain syndrome
- VernacularTitle:慢性非细菌性前列腺炎/慢性骨盆疼痛综合征患者外周血T调节细胞检测及与临床症状的相关性分析
- Author:
Shaogang WANG
;
Jian BAI
;
Qilin XI
;
Dongliang HU
;
Shiqiang SU
;
Jihong LIU
;
Zhangqun YE
- Publication Type:Journal Article
- Keywords:
Prostatitis;
T lymphocytes;
Cytokines
- From:
Chinese Journal of Urology
2008;29(12):846-849
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the role of CD4+ CDhigh25 regulatory T cells in the pathogenesis of chronic abacterial prostatitis/chronic pelvic pain syndrome (CAP/CPPS).Methods The percentage of CD4+ CD+25 and CD4+ CDhigh25 regulatory T cells was detected by flow cytometry from 45 CAP/CPPS pa-tients and 18 normal controls.The levels of interleukin-6(IL-6),IL-10,tumor necrosis factor-α(TNF-α) and transforming growth factor-β1 (TGF-β1) in serum and seminal plasma were measured by ELISA in the same cohort.Results There was no significant difference in the percentage of peripheral blood CD4+CD+25 and CD4+Cdhigh+ cells between CAP/CPPS patients and normal control (P>0.05).The ser-CD4+CD+25 and CD4+Cdhigh+ cells between CAP/CPPS patients and normal control (P>0.05>.The ser-um levels of TGF-β1 in patients with CAP/CPPS were markedly lower than those in controls (P<0.05),serum TNF-α and seminal plasma IL-6,TGF-β1 and TNF-α in CAP/CPPS patients were markedly higher than those in controls (P<0.05).There was a positive correlation between the IL-6 and the NIH-CPSI.There was also a positive correlation between the IL-10 and the pain index.In ad-dition,the percentage of peripheral blood CD+4CDhigh25 cells was positively correlated with serum TGF-β1.But the percentage of CD+4CDhigh25 cells had no correlation with ages,duration of CAP/CPPS pa-tients,NIH-CPSI and the other cytokines.Conclusions The defective function of peripheral blood CD+4CD+25 regulatory T cells may be related with the pathogenesis of CAP/CPPS.The cytokines may also play an important role in the process of pathogenesis of CAP/CPPS.
