Levels of cytokines and heat-shock protein 70 in the seminal plasma of patients with chronic bacterial prostatitis and chronic prostatitis/chronic pelvic pain syndrome.
- Author:
Hui GUO
1
;
Yue-Min XU
;
Zhang-Qun YE
;
Jian-Hua YU
Author Information
- Publication Type:Journal Article
- MeSH: Adolescent; Adult; Biomarkers; metabolism; Case-Control Studies; Cytokines; metabolism; HSP70 Heat-Shock Proteins; metabolism; Humans; Male; Middle Aged; Pelvic Pain; metabolism; Prostatitis; metabolism; Semen; metabolism; Young Adult
- From: National Journal of Andrology 2012;18(12):1088-1092
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo assess the diagnostic value and potentially protective capacity of tumor necrosis factor-alpha (TNF-alpha), interleukin 1beta (IL-1beta) and heat-shock protein 70 (HSP70) in chronic bacterial prostatitis (CBP) and chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS).
METHODSWe determined the levels of cytokines TNF-alpha, IL-1beta and HSP70 by ELISA in the seminal plasma of 150 men: 36 with CBP, 43 with CP/CPPS IIIA, 46 with CP/CPPS IIIB, and 25 healthy controls. We analyzed the correlation of the HSP70 expression in the CBP and CP/CPPS patients with the chronic prostatitis symptom index (CPSI).
RESULTSSignificantly increased levels of TNF-alpha, IL-1beta and HSP70 were observed in the seminal plasma of the CBP patients as compared with the CP/CPPS patients and healthy controls. The expression of IL-1beta was significantly higher in the patients with CP/CPPS IIIA than in those with CP/CPPS III B and the controls, while the HSP70 level remarkably lower in those with CP/CPPS than in the controls, and its concentration in the seminal plasma of the CBP patients was negatively correlated with CPSI.
CONCLUSIONThe levels of HSP70 and IL-1beta in the seminal plasma appear to be most reliable molecular biological markers for the diagnosis of CBP and CP/CPPS, respectively. HSP7O has an important protective role in the regulation of cell functions in CBP patients. CP/CPPS is probably detrimental to the function of T cells and consequently suppresses the expression of HSP70.