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P2X7R Modulates NEK7-NLRP3 Interaction to Exacerbate Experimental Autoimmune Prostatitis via GSDMD-mediated Prostate

Lei Chen1,2,3, Yi Liu1,2,3, Shaoyu Yue1,2,3

  • 1Department of Urology, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.

International Journal of Biological Sciences
|July 12, 2024
PubMed

Insights

Chronic prostatitis involves pyroptosis, a cell death process. The P2X7R-NEK7-NLRP3 pathway drives this in prostate inflammation, suggesting disulfiram as a potential treatment.

Area of Science:

  • Urology
  • Immunology
  • Cell Biology

Background:

  • Chronic prostatitis is a common urologic condition with unknown causes and limited treatments.
  • Pyroptosis, a novel cell death pathway, has an undefined role in chronic prostatitis.

Purpose of the Study:

  • To investigate the role of the P2X7R-NEK7-NLRP3 axis in pyroptosis and chronic prostatitis.
  • To explore disulfiram as a potential therapeutic agent for chronic prostatitis.

Main Methods:

  • Detected P2X7R, NEK7, and GSDMD-NT expression in human prostate tissues and EAP mice.
  • Utilized P2X7R agonists/antagonists, NLRP3 inhibitors, and disulfiram to study pyroptosis.
  • Assessed inflammatory markers and T helper 17 cell proportions.

Main Results:

  • P2X7R, NEK7, and GSDMD-NT were upregulated in inflamed prostate tissues and EAP models.
  • P2X7R activation worsened inflammation, increased NLRP3 components, and elevated Th17 cells.
  • Disulfiram treatment ameliorated EAP by inhibiting pyroptosis.

Conclusions:

  • The P2X7R-NEK7-NLRP3 axis promotes pyroptosis and chronic prostatitis development.
  • Disulfiram shows promise as an effective treatment for chronic prostatitis by targeting pyroptosis.
Keywords:
Chronic prostatitis, Prostate epithelial cellDisulfiramP2X7RPyroptosis

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