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Updated: Jun 25, 2026
Measurement of Tactile Allodynia in a Murine Model of Bacterial Prostatitis
Published on: January 16, 2013
Impact of vitamin D receptor activity on experimental autoimmune prostatitis
Ruben Darío Motrich1, Evelyne van Etten, Jos Depovere
1Centro de Investigaciones en Bioquímica Clínica e Inmunología, Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Haya de la Torre esquina Medina Allende, Ciudad Universitaria, Córdoba, Argentina.
Abstract:
Chronic non bacterial prostatitis is a chronic inflammatory syndrome. Its etiology and physiopathology are unclear and treatments are empirical and ineffective in most cases. Autoimmunity has been proposed as an etiology. In the present report, we investigated the impact of vitamin D receptor silencing, by use of VDR-KO NOD mice and the immune-modulating effect of the vitamin D3 analog TX527 on the development of Experimental Autoimmune Prostatitis in NOD mice. VDR-KO NOD mice developed a more aggressive form of autoimmune prostatitis characterized by a greater lymphoproliferative response against prostate antigen in vitro (6.92+/-4.77 vs. 2.47+/-0.41 21 days after disease induction, p<0.05) and higher levels of specific INFgamma secretion (471+/-6 vs. 386+/-5pg/ml, p<0.01). This was accompanied in vivo by more severe lesions and augmented mononuclear cell infiltration in the prostate gland. On the other hand, although analog-treated mice showed a significant reduction in the spleen T-cell specific proliferative response against prostate antigen in vitro, no effect on disease development was observed. We conclude that vitamin D receptor modulation holds the promise of interfering with autoimmune prostatitis. Introduction of more powerful analogs, or combinations with anti-T-cell reagents may represent therapeutic solutions for these group of patients.
Insights
Vitamin D receptor silencing worsens autoimmune prostatitis in mice. Vitamin D3 analog TX527 showed no effect on disease development, suggesting potential therapeutic strategies targeting vitamin D receptor modulation.
Area of Science:
- Immunology
- Endocrinology
- Urology
Background:
- Chronic non-bacterial prostatitis is an inflammatory syndrome with unclear etiology and ineffective treatments.
- Autoimmunity is a proposed cause for chronic non-bacterial prostatitis.
- Vitamin D receptor (VDR) plays a role in immune modulation.
Purpose of the Study:
- To investigate the impact of VDR silencing on experimental autoimmune prostatitis (EAP) in NOD mice.
- To evaluate the immune-modulating effect of the vitamin D3 analog TX527 on EAP development.
- To explore potential therapeutic strategies for autoimmune prostatitis.
Main Methods:
- Utilized VDR-knockout (VDR-KO) NOD mice to study VDR silencing.
- Administered vitamin D3 analog TX527 to NOD mice to assess immune modulation.
- Assessed disease severity through lymphoproliferative responses, INF-gamma secretion, prostate lesions, and mononuclear cell infiltration.
Main Results:
- VDR-KO NOD mice exhibited a more aggressive form of autoimmune prostatitis.
- VDR-KO mice showed increased lymphoproliferative response and INF-gamma secretion against prostate antigen.
- TX527 treatment reduced spleen T-cell proliferation but did not affect disease development.
Conclusions:
- Vitamin D receptor modulation shows promise in interfering with autoimmune prostatitis.
- More potent vitamin D analogs or combination therapies may offer future treatment solutions.
- Targeting VDR could be a therapeutic avenue for patients with autoimmune prostatitis.
