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Abstract: SA-PO594

C-Reactive Protein Is Renoprotective in Experimental IgA Nephropathy

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation

Authors

  • Chen, Ann, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taipei, Taiwan
  • Ka, Shuk-Man, National Defense Medical Center, Taipei, Taiwan, Taipei, Taiwan
Background

IgA nephropathy (IgAN) is the most common glomerulonephritis in the world. Although the pathogenesis of the renal disorder remains largely unknown, NLRP3 inflammasome-mediated IL-1b production and subsequent activation of adaptive immunity is implicated in the development of IgAN. C-reactive protein (CRP) is a serum biomarker for various inflammatory conditions and has been shown to inhibit the activation of the NLRP3 inflammasome.

Methods

In the present study, we examined the role that CRP could play in the evolution of IgAN using an experimental model of IgAN in CRP knockout (KO) mice, and dissected the mechanisms involved.

Results

The results show that the experimental IgAN in CRP KO mice revealed significantly increased magnitudes in (1) renal pathology, including marked mesangial cell proliferation and mononuclear leukocyte infiltration in the glomeruli and peri-glomerular interstitial tissue, (2) glomerular deposition of IgA and C3, (3) NLRP3 inflamamsome activation in the kidney, and (4) renal function impairment and proteinuria compared to their wild type (WT) counterparts equally induced of IgAN. Moreover, IL-10 levels in both sera and renal tissues were significantly elevated in IgAN in CRP KO mice, compared with WT counterparts.

Conclusion

In conclusion, CRP may serve as a protective role in the development of IgAN by inhibiting NLRP3 inflammasome and enhancing the production of IL-10. The results suggest that CRP may be a potential therapeutic agent for IgAN.

Funding

  • Government Support - Non-U.S.