Login to Access Video or Poster Abstract: MP13-19
Sources of Funding: NIDDK U54 DK112079

Introduction

Discovery of serum biomarkers for benign prostatic hyperplasia (BPH) is strongly pursued by the MTOPSProstatic Samples Analysis (MPSA) Consortium and other groups in order to discriminate BPH-related pathologies, identify risk of progressive disease; and personalized management of BPH-related LUTS. Compared to serum, urine collected non-invasively by the patient himself has obvious advantages as a suitable matrix for BPH biomarker discovery. Besides, proximity to prostate can permit selective contribution of BPH related proteins into urine. Here, we compared the distribution of prostatic inflammation mediators in the two biofluids obtained from a rat model.

Methods

Non-bacterial prostatic inflammation was induced by intraprostatic injection of formalin (50μL) or saline (sham) in three month- old male Sprague-Dawley rats (n=4 in each group). 12 hour night time urination pattern were noted in metabolic cage a day before injection and 7 days later. Urine and serum collected on 7th day was frozen prior to simultaneous multiplex analysis of 27 proteins using a MILLIPLEX MAP Rat Cytokine/Chemokine Panel kit (Millipore, Billerica, MA).

Results

Attached figure demonstrates that EGF, GM-CSF, IFN-γ, IL-1?, IL-10, IL-18 and eotaxin were abundant in urine, while undetectable in serum. Paired analysis of urine and serum levels from sham group against the levels of prostatitis group referred to as urine-P and serum-P, respectively found that VEGF, IL-1α, IL-4, CXCL-10 and CX3CL1 were elevated in urine-P, whereas IL-5 and CCL5 were elevated in serum-P (*p<0.05). Levels of CXCL-5, IL-12p70, CCL2, CCL3, G-CSF, TNF-α and Leptin were comparable in the biofluids of both groups. Significantly decreased levels of CXCL-10 and CX3CL-1 in serum of prostatitis group (#p<0.05) is linked to their commensurate increase in urine-P, which also showed slightly elevated IL-6, IL-13 and IL-17A.

Conclusions

Majority of the mediators driving prostatic inflammation were abundant in urine, while several of the mediators were undetectable in serum. Whether this discordance in the biofluids is linked to the increased proteolysis of chemokines in serum or to the exclusive secretion of chemokines from prostate into urine needs to be studied. Urine is a reliable matrix for the discovery of potential non-invasive biomarkers for the routine clinical management of BPH.

Funding

NIDDK U54 DK112079