Prostate specific antigen and prostatitis II. PSA production and release kinetics in vitro

Abstract

Elevations in serum prostate specific antigen (PSA) levels in patients with prostatitis are well known, but the pathophysiologic mechanisms involved with this phenomenon are poorly understood. We have recently evaluated the effect of prostatitis on PSA levels in primates. This data demonstrated a rapid rise in PSA, which subsequently fell along the biological decay curve. This suggested a release of sequestered PSA. We evaluated the effect of infection upon PSA production for the prostatic adenocarcinoma cell line LNCaP. The cell line was determined to produce 9.6 +/- 2.7 fg/cell/hr PSA with essentially linear kinetics. No effect was seen with dead bacteria, bacterial supernatant or complement upon the PSA production. Live E. coli had no effect for 4-8 hours at which time the cells sloughed and PSA production ceased. No release of stored PSA was seen. These data do not elucidate the reasons for increased serum PSA levels found with acute bacterial prostatitis, but indicate that it is not a storage phenomenon.

Prostatitis and serum prostate-specific antigen

“…It has been shown that the human prostate cancer cell line LNCaP, when infected with live E. coli bacteria or when treated with heat-killed bacteria or lipo-polysaccharide and bacterial culture supernatants in vitro, did not lead to an increased expression of PSA [20]. This suggested that these bacterial factors did not lead to an increased synthesis of PSA.…”

Effect of Inflammation and Benign Prostatic Enlargement on Total and Percent Free Serum Prostatic Specific Antigen

“…Brawn et al [10]reported that in 105 autopsy cases, 50% of the cases with a serum PSA higher than 4.0 ng/ml had acute or chronic prostatitis compared to 22% without inflammation. Moon et al [11]did not observe an increase in PSA production in LNCaP cell line when infected with bacteria in vitro, and they suggested that infection and inflammation would increase serum PSA concentrations by affecting the natural anatomical and physiological barriers to PSA diffusion between the prostatic glandular tissue and the bloodstream.…”

Prostatitis and serum prostate-specific antigen

“…It has been shown that the human prostate cancer cell line LNCaP, when infected with live E. coli bacteria or when treated with heat-killed bacteria or lipo-polysaccharide and bacterial culture supernatants in vitro, did not lead to an increased expression of PSA [20]. It has been shown that the human prostate cancer cell line LNCaP, when infected with live E. coli bacteria or when treated with heat-killed bacteria or lipo-polysaccharide and bacterial culture supernatants in vitro, did not lead to an increased expression of PSA [20].…”