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Published on: January 16, 2013
Prostate-derived IL-1β upregulates expression of NMDA receptor in the paraventricular nucleus and shortens
Jie Yang1, Jiao-Chen Luan1, Jian-Huai Chen2
1Department of Urology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210008, China.
Abstract:
Experimental autoimmune prostatitis (EAP)-induced persistent inflammatory immune response can significantly upregulate the expression of N-methyl-D-aspartic acid (NMDA) receptors in the paraventricular nucleus (PVN). However, the mechanism has not yet been elucidated. Herein, we screened out the target prostate-derived inflammation cytokines (PDICs) by comparing the inflammatory cytokine levels in peripheral blood and cerebrospinal fluid (CSF) between EAP rats and their controls. After identifying the target PDIC, qualified males in initial copulatory behavior testing (CBT) were subjected to implanting tubes onto bilateral PVN. Next, they were randomly divided into four subgroups (EAP-1, EAP-2, Control-1, and Control-2). After 1-week recovery, EAP-1 rats were microinjected with the target PDIC inhibitor, Control-1 rats were microinjected with the target PDIC, while the EAP-2 and Control-2 subgroups were only treated with the same amount of artificial CSF (aCSF). Results showed that only interleukin-1β(IL-1β) had significantly increased mRNA-expression in the prostate of EAP rats compared to the controls (P < 0.001) and significantly higher protein concentrations in both the serum (P = 0.001) and CSF (P < 0.001) of the EAP groups compared to the Control groups. Therefore, IL-1β was identified as the target PDIC which crosses the blood-brain barrier, thereby influencing the central nervous system. Moreover, the EAP-1 subgroup displayed a gradually prolonged ejaculation latency (EL) in the last three CBTs (all P < 0.01) and a significantly lower expression of NMDA NR1 subunit in the PVN (P = 0.043) compared to the respective control groups after a 10-day central administration of IL-1β inhibitors. However, the Control-1 subgroup showed a gradually shortened EL (P < 0.01) and a significantly higher NR1 expression (P = 0.004) after homochronous IL-1β administration. Therefore, we identified IL-1β as the primary PDIC which shortens EL in EAP rats. However, further studies should be conducted to elucidate the specific molecular mechanisms through which IL-1β upregulates NMDA expression.
Insights
Experimental autoimmune prostatitis increases interleukin-1β (IL-1β), a prostate-derived inflammation cytokine, which affects ejaculation latency and N-methyl-D-aspartic acid (NMDA) receptor expression in the brain. This study identifies IL-1β as a key factor in prostatitis-related sexual dysfunction.
Area of Science:
- Neuroscience
- Immunology
- Reproductive Biology
Background:
- Persistent inflammation from experimental autoimmune prostatitis (EAP) upregulates N-methyl-D-aspartic acid (NMDA) receptors in the paraventricular nucleus (PVN).
- The precise mechanism linking EAP-induced inflammation to NMDA receptor changes remains unclear.
Purpose of the Study:
- To identify prostate-derived inflammation cytokines (PDICs) involved in EAP.
- To investigate the role of identified PDICs in regulating ejaculation latency (EL) and NMDA receptor expression in the PVN.
Main Methods:
- Compared inflammatory cytokine levels in blood and cerebrospinal fluid (CSF) between EAP and control rats.
- Administered IL-1β inhibitors or IL-1β to the PVN of EAP and control rats.
- Assessed copulatory behavior testing (CBT) and NMDA NR1 subunit expression in the PVN.
Main Results:
- Interleukin-1β (IL-1β) was identified as the primary PDIC, showing increased expression in EAP rats and crossing the blood-brain barrier.
- IL-1β inhibition in EAP rats prolonged ejaculation latency and decreased NMDA NR1 subunit expression in the PVN.
- Direct IL-1β administration to control rats shortened ejaculation latency and increased NR1 expression.
Conclusions:
- IL-1β is a key prostate-derived inflammation cytokine that influences ejaculation latency and NMDA receptor expression in the PVN.
- IL-1β plays a significant role in the sexual dysfunction associated with experimental autoimmune prostatitis.
- Further research is needed to fully elucidate the molecular mechanisms of IL-1β-induced NMDA upregulation.
