Experimental autoimmune prostatitis induces microglial activation in the spinal cord

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.