Basic scienceNerve growth factor and chronic prostatitis/chronic pelvic pain syndrome☆
Section snippets
Patient populations
All patients met the National Institutes of Health criteria for nonbacterial chronic prostatitis category III.6 Forty-eight patients with prostatitis underwent a basic history and physical examination by a physician, including a digital rectal examination and expressed prostatic secretions if obtainable. In addition, 14 normal male controls were recruited. Volunteers were examined by a physician and had no history of genitourinary symptoms, instrumentation, or surgery.
At the time of the
Cytokine levels in seminal plasma
For the present study, we established the presence of NGF and the pro-inflammatory cytokine IL-6 in the seminal plasma of the CPPS and control populations. These levels were compared with levels of the pro-inflammatory cytokines IL-8 and IFN-gamma, the immunoregulatory cytokine IL-2, and the anti-inflammatory cytokine IL-10 from the same patient population, as previously reported.3 The seminal plasma cytokines (NGF, IL-6, IL-8, IFN-gamma, IL-2, and IL-10) were all detectable in most of the CPPS
Comment
Chronic prostatitis is a complex condition of unknown etiology and pathogenesis. Currently, nothing is known about the presence or potential role of NGF in CPPS. Evidence suggests that NGF can induce and/or alter sensitivity to pain. For example, studies have indicated that NGF may be an important mediator of some forms of persistent pain and that NGF can alter pain-related behavior.10 In fact, a single dose of 1 mg/mL of NGF administered to animals resulted in increased sensitivity to both
Conclusions
Our studies have demonstrated that in patients with CPPS, increased pain is associated with increased seminal plasma IL-10 and NGF expression, but decreased IL-6 expression. We believe our present data support a model of tissue regulation in which chronic injury and inflammation to the prostate results in the expression of pro-inflammatory cytokines (IL-6 and IL-8) that, in response, leads to the expression of the anti-inflammatory cytokine IL-10. Although this IL-6/IL-8-induced expression of
Acknowledgements
To Drs. Scott Matson, Jeff Wong, and Willie Underwood for their help in recruiting patients.
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These studies were supported in part by grant DK-52718 from the National Institutes of Health.