Immunological alterations in the ejaculate of chronic prostatitis patients: clues for autoimmunity.
The aim of this prospective study was to observe immunophenotypic patterns in the ejaculate of patients with noninflammatory chronic pelvic pain syndrome (Cat IIIB CPPS) and to test for a possible autoimmune aetiology. Thirty-five patients of a total of 88 patients with chronic prostatitis Cat IIIB were consecutively selected. Monthly ejaculate testing was carried out for IgG, IgA, IgM, IL-1alpha, sIL-2R and IL-6. The control group for ejaculate analysis was composed of 96 normal ejaculates (according to the WHO criteria). Immunohistochemical detection of CD3 cells (T lymphocytes) and CD20 cells (B lymphocytes) was performed in 71 biopsy cylinders of Cat IIIB CPPS patients and in 25 prostate biopsy cylinders of subjects without symptoms or obstruction. Intra-acinar T-lymphocytic infiltrates were dominated by T-cytotoxic cells (P = 0.05). Ejaculate IL-6 and ejaculate IgA increased significantly and dropped again, correlating with a release of clinical symptoms. Inflammatory ejaculate interleukin concentrations correlated with the immunohistochemical findings with presence of large numbers of T cells (all P-values < or = 0.01). Immunomodulation was performed in a pilot series of three patients by five monthly cycles of IgG (Sandoglobulin), 1 g kg-1 body weight. Immunomodulation with IgG decreased pain moderately and did not change ejaculate interleukin and immunoglobulin concentrations. In summary, interleukin and immunoglobulin determinations in the ejaculate revealed an inflammatory process even in Cat IIIB CPPS. The findings of intra-acinar T-cell rich infiltrates and the associated inflammatory reaction may indicate a possible autoimmune component in the aetiology of CPPS. Exact origin and role of interleukin changes in the ejaculate of CPPS patients need to be further evaluated. Unfortunately, pilot series with immunomodulation with IgG do not seem to provide clear clinical benefit.
John
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H
Clinic of Urology, University Hospital and University of Zürich, Zürich, Switzerland. john@uro.usz.ch
Maake
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Barghorn
A
A
Zbinden
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Hauri
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D
Joller-Jemelka
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HI
D000328:Adult; D018951:Antigens, CD20 / Q000032:analysis; D015551:Autoimmunity; D001402:B-Lymphocytes / Q000276:immunology / Q000473:pathology; D017252:CD3 Complex / Q000032:analysis; D018414:CD8-Positive T-Lymphocytes / Q000473:pathology; D002908:Chronic Disease; D006801:Humans; D007070:Immunoglobulin A / Q000032:analysis; D007074:Immunoglobulin G / Q000032:analysis; D007150:Immunohistochemistry; D015850:Interleukin-6 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D011467:Prostate / Q000473:pathology; D011472:Prostatitis / Q000145:classification / Q000276:immunology* / Q000473:pathology; D015375:Receptors, Interleukin-2 / Q000032:analysis; D012661:Semen / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology
D018951:Antigens, CD20; D017252:CD3 Complex; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D015850:Interleukin-6; D015375:Receptors, Interleukin-2