Related Experiment Video
Updated: Apr 23, 2026
Measurement of Tactile Allodynia in a Murine Model of Bacterial Prostatitis
Published on: January 16, 2013
Experimental autoimmune prostatitis induces microglial activation in the spinal cord
Larry Wong1, Joseph D Done, Anthony J Schaeffer
1Department of Urology, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Background:
The pathogenesis of chronic prostatitis/chronic pelvic pain syndrome is unknown and factors including the host's immune response and the nervous system have been attributed to the development of CP/CPPS. We previously demonstrated that mast cells and chemokines such as CCL2 and CCL3 play an important role in mediating prostatitis. Here, we examined the role of neuroinflammation and microglia in the CNS in the development of chronic pelvic pain.
Methods:
Experimental autoimmune prostatitis (EAP) was induced using a subcutaneous injection of rat prostate antigen. Sacral spinal cord tissue (segments S14-S5) was isolated and utilized for immunofluorescence or QRT-PCR analysis. Tactile allodynia was measured at baseline and at various points during EAP using Von Frey fibers as a function for pelvic pain. EAP mice were treated with minocycline after 30 days of prostatitis to test the efficacy of microglial inhibition on pelvic pain.
Results:
Prostatitis induced the expansion and activation of microglia and the development of inflammation in the spinal cord as determined by increased expression levels of CCL3, IL-1β, Iba1, and ERK1/2 phosphorylation. Microglial activation in mice with prostatitis resulted in increased expression of P2X4R and elevated levels of BDNF, two molecular markers associated with chronic pain. Pharmacological inhibition of microglia alleviated pain in mice with prostatitis and resulted in decreased expression of IL-1β, P2X4R, and BDNF.
Conclusion:
Our data show that prostatitis leads to inflammation in the spinal cord and the activation and expansion of microglia, mechanisms that may contribute to the development and maintenance of chronic pelvic pain.
Insights
Neuroinflammation and microglia activation in the spinal cord contribute to chronic pelvic pain in prostatitis. Inhibiting microglia reduced pain and associated molecular markers, suggesting a therapeutic target.
Area of Science:
- Neuroscience
- Immunology
- Pain Research
Background:
- The exact causes of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) remain unclear.
- Previous research implicated immune responses and the nervous system in CP/CPPS development.
- Mast cells and chemokines (CCL2, CCL3) are known contributors to prostatitis.
Purpose of the Study:
- To investigate the role of neuroinflammation and microglia in the central nervous system (CNS).
- To understand their contribution to the development of chronic pelvic pain associated with prostatitis.
Main Methods:
- Experimental autoimmune prostatitis (EAP) was induced in rats.
- Sacral spinal cord tissue was analyzed using immunofluorescence and QRT-PCR.
- Tactile allodynia was measured to assess pelvic pain.
- Minocycline was used to inhibit microglia and evaluate its effect on pain.
Main Results:
- Prostatitis led to microglia expansion, activation, and spinal cord inflammation (increased CCL3, IL-1β, Iba1, ERK1/2 phosphorylation).
- Microglial activation elevated P2X4R and BDNF, markers linked to chronic pain.
- Minocycline treatment reduced pain and decreased IL-1β, P2X4R, and BDNF expression.
Conclusions:
- Prostatitis induces spinal cord inflammation and microglia activation.
- These neuroinflammatory mechanisms may drive the development and persistence of chronic pelvic pain.
- Targeting microglia may offer a therapeutic strategy for chronic pelvic pain.
More Related Videos
05:44Author Spotlight: Creating a Versatile Experimental Autoimmune Encephalomyelitis Model Relevant for Both Male and Female Mice
Published on: October 13, 2023
09:20Implanting Glass Spinal Cord Windows in Adult Mice with Experimental Autoimmune Encephalomyelitis
Published on: December 21, 2013