The Role of MCP 1 and IL 6 on the Progress of Crescentic Glomerulonephritis / 대한신장학회지
Korean Journal of Nephrology
;
: 326-334, 2009.
Artigo
em Inglês
| WPRIM
| ID: wpr-84132
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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Proteinúria
/
Autoanticorpos
/
Membrana Basal
/
Fibrose
/
Fatores de Crescimento Transformadores
/
Citocinas
/
Fibronectinas
/
Interleucinas
/
Interferons
/
Interleucina-6
Limite:
Animais
Idioma:
Inglês
Revista:
Korean Journal of Nephrology
Ano de publicação:
2009
Tipo de documento:
Artigo
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