MP19-15 PROSTATIC INFLAMMATION TRIGGERS VOIDING DYSFUNCTION BY NEURAL CROSS-TALK.

Abstract

You have accessJournal of UrologyBenign Prostatic Hyperplasia: Basic Research1 Apr 2014MP19-15 PROSTATIC INFLAMMATION TRIGGERS VOIDING DYSFUNCTION BY NEURAL CROSS-TALK. Sanghee Lee, Guang Yang, Jerry Gipp, and Wade Bushman Sanghee LeeSanghee Lee More articles by this author , Guang YangGuang Yang More articles by this author , Jerry GippJerry Gipp More articles by this author , and Wade BushmanWade Bushman More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2014.02.716AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES A high incidence of prostatic inflammation in patients with benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS) has been previously reported. We postulate that prostatic inflammation sensitizes afferent fibers from the bladder resulting in changes in bladder function. We show here that afferent innervation of the bladder and prostate originate from overlapping groups of dorsal root ganglia and that prostatic inflammation induces increased urinary frequency. METHODS A retro-grade neuro-tracer Fast Blue was applied to each of the prostate lobes, anterior, dorsal-lateral and ventral as well as the seminal vesicle and bladder in adult C57BL/6 mice. Tissues including pelvic organs and DRGs were harvested at post-application day 7. Prostatic inflammation was induced by trans-urethral instillation of uropathogenic E.coli 1677. Cystitis was prevented by continuous administration of nitrofurantoin (NTF). We performed metabolic cage tests to determine voiding behavior, while using H&E staining and bacterial culture to validate our animal model. RESULTS Our study clearly demonstrates that prostate and bladder share afferent innervation via convergent DRGs in spinal segment T13, L1, L2, L6 and S1. Mice inoculated with E.coli + NTF exhibited bacterial infection and intense inflammation in the prostate while the bladder exhibited neither bacterial infection nor evidence of inflammation. Mice in E.coli + NTF group showed significantly increased voiding frequency and decreased volume per void as compared to a control group. CONCLUSIONS These observations support the hypothesis that prostatic inflammation can induce abnormal voiding behavior by pelvic cross-sensitization. © 2014FiguresReferencesRelatedDetails Volume 191Issue 4SApril 2014Page: e194 Advertisement Copyright & Permissions© 2014MetricsAuthor Information Sanghee Lee More articles by this author Guang Yang More articles by this author Jerry Gipp More articles by this author Wade Bushman More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...