The Role of MCP 1 and IL 6 on the Progress of Crescentic Glomerulonephritis.
- Author:
Hyewon HAHN
1
;
Eun Young UM
;
Il Soo HA
Author Information
1. Department of Pediatrics, Eulji University School of Medicine, Korea. petercat67@gmail.com
- Publication Type:Original Article
- Keywords:
Anti-glomerular basement membrane disease;
Fibrosis;
Interleukin-6;
Monocyte chemoattractant protein-1
- MeSH:
Animals;
Anti-Glomerular Basement Membrane Disease;
Autoantibodies;
Basement Membrane;
Chemokine CCL2;
Collagen Type III;
Cytokines;
Extracellular Matrix;
Fibronectins;
Fibrosis;
Glomerulonephritis;
Interferons;
Interleukin-12;
Interleukin-18;
Interleukin-6;
Interleukins;
Kidney;
Mice;
Nephritis;
Proteinuria;
Real-Time Polymerase Chain Reaction;
Transforming Growth Factors
- From:Korean Journal of Nephrology
2009;28(4):326-334
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Growing data on the relationship between cytokine expression and the progression of renal diseases make these cytokines potential targets for therapeutic interventions. Weexamined the helper T1-cell- and macrophage-associated cytokines in anti-glomerular basement membrane (GBM) antibody-induced nephritis in mice and their temporal relationships with renal tissue fibrosis. METHODS: Kidneys were harvested on days 1, 3, 7, 11, and 16 after glomerulonephritis was induced with anti-GBM antibody. The progression of renal fibrosis was serially monitored to quantitate the accumulation of cortical extracellular matrix, and various cytokines were measured simultaneously. RESULTS: A single injection of anti-GBM antibody successfully produced severe crescentic glomerulonephritis. Proteinuria increased abruptly and both mesangial matrix expansion and interstitial fibrosis progressed rapidly. Cortical fibronectin and type III collagen increased continuously, reaching a peak on day 7, and the deposition of type III collagen followed the same pattern, in parallel with that of urinary transforming growth factor 1 (TGF-1) expression. Serial cytokine measurements revealed a sustained increase in interleukin (IL) 6 and monocyte chemoattractant protein 1 (MCP1) from day 3, but neither IL12, IL18, nor interferon changed significantly. Real-time polymerase chain reaction confirmed these features at the transcription level. CONCLUSION: MCP1 and IL6 correlated with the progression of renal fibrosis, with no increase in Th1- inducing cytokines. This confirms MCP1 and IL6 as attractive therapeutic targets for renal fibrosis in crescentic glomerulonephritis.
