INTRODUCTIONChronic abacterial prostatitis and prostatodynia (now referred to as CPPS types IIIa and IIIb, respectively, in the NIH classification [1]) are poorly understood conditions, which are insufficiently recognized [2]. They are surprisingly common and account for approximately 8% of visits to urologists in the United States. They affect men in all age groups but primarily those in the age group 36-50 years [3]. It has been documented that the impairment to quality of life from chronic prostatitis compares with that due to myocardial infarction, angina and Crohn's disease [4].Controversy exists concerning the aetiology of this condition. Current investigation has focused largely on a microbial or an autoimmune cause, though the two are not mutually exclusive. To investigate a microbial cause, investigators have used PCR to amplify microbial 16S rRNA genes from prostatic biopsies. Kreiger et al. demonstrated microbial 16S rRNA in 77% of the prostates of men with chronic prostatitis but did not investigate a control group [5]. A subsequent paper by Keay et al. found the 16S rRNA in the prostates of 8/9 men with prostate cancer (although this group had previously had trans-rectal biopsies) [6]. Hochreiter [7] found no 16S rRNA gene product in the stored prostates of 18 men whose prostates had been preserved at the time of organ donation and in whom there was no information on whether they had any prostatitis symptoms ante-mortem. In a subsequent study Kreiger found the 16S rRNA gene product in 20% of 107 patients with prostate cancer as compared to 46% of 170 men with chronic prostatitis. The median age of the men with prostate cancer was 64 and the median age of the men with prostatitis was 38 [8]. Essentially it is difficult to obtain aged matched controls to undergo a prostatic biopsy.The autoimmune hypothesis suggests that types IIIa and IIIb prostatitis (CPPS) are caused by autoimmune mediated injury to the genital tract (including the prostate), which is precipitated by genitourinary inflammatory events such as urinary tract infection (UTI), acute bacterial prostatitis, urethritis and repetitive trauma. The male genital tract is an immune privileged site [9], and seminal plasma is highly immunosuppressive due to high concentrations of PGE 2 [10] in the semen. The seminal plasma is also capable of being recognized by the immune system. Halpern first described seminal plasma allergy in 1967 [11] in a woman who experienced postcoital anaphylaxis. Other authors have reported similar findings and suggested that the allergic component was a protein(s) in the range of 20-40 KD [12,13]. An antigen does not need to be produced by the prostate for the prostate to be affected as intraprostatic spermatozoa have been found on postmortem analysis [14] mainly in the peripheral zone.The finding of increased levels of IgA and IgG in the expressed prostatic secretion of patients with abacterial prostatitis, compared to controls, supports an autoimmune aetiology for this condition, since this Ig was not specific for know...