Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3903002 | Urology | 2010 | 5 Pages |
ObjectivesTo identify the characteristics of circulating CD4+CD25high regulatory T cells in chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). We sought to discover the possible mechanism underlying induction of CP/CPPS by autoimmune factors.MethodsA total of 69 men with CP/CPPS and 25 age-matched, asymptomatic controls underwent quantification of peripheral blood CD4+CD25high regulatory T cells, using flow cytometry, followed by measurement of interleukin (IL)-6, IL-10, tumor necrosis factor-α (TNF-α), and transforming growth factor-β1 (TGFβ1) in serum, and forkhead box P3 (FOXP3) mRNA level in peripheral blood mononuclear cells, using enzyme-linked immunosorbent assay and real-time quantitative reverse transcriptase-polymerase chain reaction, respectively.ResultsThe FOXP3 gene mRNA level in CP/CPPS patients was significantly lower than that in controls. Serum TNF-α level increased but the TGFβ1 level decreased in CP/CPPS patients. No change was observed in the levels of IL-6 and IL-10. However, there was normal frequency of CD4+CD25high T cells in CP/CPPS patients. No differences were observed in expression of FOXP3 and serum cytokines and population of CD4+CD25high T cells between CP/CPPS IIIA and IIIB patients. In addition, statistically significant correlation was only found between serum IL-6 production and national institutes of health-chronic prostatitis symptom index total score of CP/CPPS patients. The frequency of CD4+CD25high T cells and FOXP3 expression level did not correlate with age, duration, and total national institutes of health-chronic prostatitis symptom index score of CP/CPPS patients.ConclusionsFOXP3 and serum cytokines, such as TNF-α and TGFβ1, might be important for the pathogenesis of CP/CPPS and possibly affect the suppressive function of CD4+CD25high regulatory T cells. This influence may result in the onset of CP/CPPS, but its assessment requires further study.