Effect of inflammation on prostatic protein synthesis and luminal secretion in vivo.

PURPOSE: Inflammation of the prostate, or prostatitis, can be caused by an infectious process or can occur in a reportedly non-bacterial form, the etiology of which is largely unknown. The present study was undertaken to establish a method of studying prostatic protein synthesis and secretion in vivo and determine the effects of lipopolysaccharide (LPS)-induced prostatic inflammation on these processes.
MATERIALS AND METHODS: Sprague-Dawley rats were divided into three groups: control, 24 hours LPS-inflammation, and 24 hours LPS + antibody against tumor necrosis factor (anti-TNF). 35S-methionine was perifused in vivo around ventral prostate ducts for 3 hours. Ductal fluid (DF) was collected by micropuncture and ductal extract (DE) was collected by tissue homogenization. DE and DF were then subjected to SDS-PAGE and autoradiography. Densitometric analysis of gels and autoradiograms was used to compare protein synthesis (total DE 35S-proteins) and protein secretion (DF 35S-proteins) among the three groups. RESULTS AND
CONCLUSIONS: The method proved to be effective for studying prostatic protein synthesis and secretion in vivo. LPS-induced inflammation caused an increase in total 35S-proteins in both the DE and the DF when compared with controls. There were significant increases in both the total number of proteins produced as well as the densitometric quantity of protein in the inflamed group. Some specific prostatic proteins were also upregulated by inflammation. The addition of anti-TNF did not significantly alter inflammation-induced protein synthesis or secretion at the time/dose studied.