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IL17 Mediates Pelvic Pain in Experimental Autoimmune Prostatitis (EAP).

Stephen F Murphy¹, Anthony J Schaeffer¹, Joseph Done¹

¹Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States of America.

|May 2, 2015

Summary

Chronic pelvic pain syndrome (CPPS) involves immune system dysfunction. Research shows Interleukin-17 (IL-17) drives pain development in experimental autoimmune prostatitis (EAP), a CPPS model.

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Area of Science:

Immunology
Urology
Pain Research

Background:

Chronic pelvic pain syndrome (CPPS) is the most common prostatitis diagnosis, characterized by unknown etiology and limited treatments.
Inflammatory mediators, including cytokines and chemokines, correlate with CPPS symptom severity.
Altered adaptive immunity and autoimmunity are hypothesized to contribute to CPPS pathogenesis.

Purpose of the Study:

To investigate the role of CD4+ T-cell subsets in the development and maintenance of prostate pain using a mouse model.
To explore the therapeutic potential of targeting IL-17 in experimental autoimmune prostatitis (EAP).
To identify novel cytokines associated with CPPS symptom severity.

Main Methods:

Utilized the experimental autoimmune prostatitis (EAP) mouse model of CPPS.
Employed tactile allodynia behavioral testing and flow cytometry to assess pain and immune cell populations.
Administered prophylactic and therapeutic anti-IL17 antibody treatments.

Main Results:

Increased CD4+IL17A+ T-cells were observed upon EAP induction.
Prophylactic anti-IL17 treatment prevented pelvic pain onset in EAP mice.
Therapeutic IL-17 blockade did not reverse established pain, indicating IL-17's role in pain development, not maintenance.
Elevated IL-7 levels correlated with increased symptom severity in CPPS patients and EAP mice.

Conclusions:

CD4+IL17+ T-cells play a critical role in the development of chronic pelvic pain in the EAP model.
IL-17 is essential for the initiation but not the maintenance of chronic pain in EAP.
IL-7 is a potential biomarker for CPPS symptom severity and may contribute to autoimmune T-cell responses.