Moderated Poster

Poster, Podium & Video Sessions

MP11-07: Clinically isolated gram-positive prostate bacteria induce chronic pelvic pain.

Friday, May 12
1:00 PM - 3:00 PM
Location: BCEC: Room 151

Presentation Authors: Stephen Murphy, Jonathan Anker, Anthony Schaeffer, Praveen Thumbikat*, Chicago, IL

Introduction: Gram-positive bacterial strains comprise the most common isolates found in both healthy and CPPS patient samples. The role of these bacteria in development and maintenance of pain in CPPS is unknown

Methods: Gram-positive bacteria were isolated from the prostates, i. e. bacteria count was 1 log greater in the EPS or VB3 than that in the VB1 and VB2, of three CPPS patients (pain inducers, PI) and one from a healthy volunteer (non-pain inducer, NPI). The bacteria were inoculated intra-urethrally in two genetic mouse backgrounds and analyzed for their ability to induce tactile allodynia and to colonize the murine prostate.

Results: PI strains (Staphylococcus haemolyticus 2551, Enterococcus faecalis 427 and Staphylococcus epidermidis 7244) were capable of inducing and maintaining robust tactile allodynia responses (200% increase above baseline) for 28 days initiating at day 7 post-infection in NOD/ShiLtJ mice. Conversely the healthy subject derived strain (Staphylococcus epidermidis NPI) demonstrated no significant pain responses above baseline at any time-point examined (Days 7, 14, 21, 28). Intra-urethral inoculation of any of the four bacterial strains into C57BL/6 mice did not induce significant increases in pain responses above baseline. In vitro adherence and invasion assays revealed no significant difference between strains to invade WPMY or RWPE-1 cells. E. faecalis 427 demonstrated a reduced capacity for intracellular proliferation in WPMY but not RWPE-1 cells compared to the other strains. In vivo, colony counts were also performed on prostate tissues removed from both NOD/ShiLtJ and C57BL/6 mice at day 28 post-infection. All bacterial strains colonized equally well comparing within mouse background including NPI. Significant differences were observed however when comparing the bacterial loads of NOD/ShiLtJ and C57BL/6 mice.

Conclusions: Gram-positive isolates from the prostates of CPPS patients showed dramatically enhanced ability to induce tactile allodynia compared to taxonomically similar gram-positive strain isolated from a healthy control subject. Pain responses were shown to be dependent on the genetic background of the host and not on in vivo colonization differences between strains. All four strains demonstrated similar growth, invasion and proliferation responses in vitro, strongly implicating host:pathogen interactions in development of pain.

Source Of Funding: NIH R01DK094898, R01DK108127.

Praveen Thumbikat, DVM, PhD

Northwestern University

Praveen Thumbikat, DVM, PhD
O'Connor Family Research Professor of Urology
Associate Professor of Urology and Pathology
Northwestern University Feinberg School of Medicine
I am an academic researcher with a major focus on the immune basis of prostate disease in humans. We have a particular emphasis on chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), a debilitating medical condition characterized by dysuria and pelvic pain. My laboratory is also very interested in understanding the mechanism underlying inflammation of the human prostate and it's impact on benign disease and carcinogenesis. My laboratory utilizes comparative animal models that closely track human prostate disease as tools for translational research. Some specific areas of research interest are as follows - 1. Th1/Th17 mechanisms in chronic pelvic pain: We are interested in understanding the mechanism of T cell mediated pain, the effectors of the pain pathway and measures to modulate Th1/Th17 immune response in animal models and ultimately in humans. 2. Mast cell mediated mechanisms in chronic pelvic pain and LUTS: We study the role of mast cells in pelvic pain and LUTS by focusing on neuroimmune mechanisms as well as fibrosis.


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MP11-07: Clinically isolated gram-positive prostate bacteria induce chronic pelvic pain.

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