4.6 Article

Prostate Secretions From Men With Chronic Pelvic Pain Syndrome Inhibit Proinflammatory Mediators

期刊

JOURNAL OF UROLOGY
卷 184, 期 4, 页码 1536-1542

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1016/j.juro.2010.05.086

关键词

prostate; prostatitis; pain; chemokines; inflammation

资金

  1. National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases [5U01DK065277-05, 1K01 DK079019-01A2]
  2. National Institutes of Health [AR055240, AR056099]
  3. Haymarket Media
  4. NovaBay Pharmaceuticals
  5. American Medical Systems
  6. J. Reckner Associates
  7. Pfizer
  8. Propagate Pharma
  9. Hagen/Sinclair Research Recruiting and American Urological Association

向作者/读者索取更多资源

Purpose: In the past numerous chemokines have been noted in the expressed prostatic secretions of patients with chronic prostatitis/chronic pelvic pain syndrome. We examined the functional effects of chemokines in expressed prostatic secretions of patients with chronic pelvic pain syndrome. Materials and Methods: We studied the functional effects of expressed prostatic secretions on human monocytes by examining monocyte chemotaxis in response to monocyte chemoattractant protein-1, a major chemoattractant previously identified in chronic prostatitis/chronic pelvic pain syndrome cases. We determined effects on cellular signaling by quantifying intracellular calcium increase in monocytes and nuclear factor-kappa B activation in normal prostate epithelial cells. Results: Results show that the monocyte chemoattractant protein-1 in expressed prostatic secretions is nonfunctional with an inability to mediate human monocyte chemotaxis, or mediate signaling in monocytes or prostate epithelial cells. This lack of functionality could be extended to other proinflammatory cytokines, such as interleukin-1 beta and tumor necrosis factor-alpha, when incubated with expressed prostatic secretions from patients with chronic pelvic pain syndrome. The mechanism underlying this apparent ability to modulate proinflammatory cytokines involves heat labile extracellular proteases that mediate the inhibition of immune and prostate epithelial cell function. Conclusions: These results may have implications for the design of specific diagnostic and therapeutic methods targeted toward the complete resolution of prostate inflammatory insults.

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