Suppression of experimental crescentic glomerulonephritis by the interleukin-1 receptor antagonist View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1993-02

AUTHORS

H Y Lan, D J Nikolic-Paterson, M Zarama, J L Vannice, R C Atkins

ABSTRACT

The role of interleukin-1 (IL-1) in the pathogenesis of experimental crescentic glomerulonephritis was investigated. Administration of the interleukin-1 receptor antagonist (IL-1ra) was used to block the action of IL-1 during disease development. Two groups of six rats were primed with rabbit IgG, followed five days later by injection of rabbit anti-GBM serum (day 0). Animals were treated with a constant infusion of recombinant human IL-1ra (plasma level approximately 100 to 200 ng/ml) or saline (untreated) from day -1 until being killed on day 14. Untreated animals exhibited severe proteinuria and development renal dysfunction shown by increased serum urea and serum creatinine and reduced creatinine clearance. In contrast, IL-1ra treated animals had significantly reduced proteinuria (IL-1ra vs. untreated, P < 0.05) and maintained normal renal function (IL-1ra vs. untreated, P < 0.05). Histologically, IL-1ra treatment markedly reduced glomerular hypercellularity, glomerular necrosis and crescent formation and almost completely abrogated tubular atrophy and fibrosis. IL-1ra treatment suppressed glomerular macrophage accumulation by 57% (P < 0.01), while macrophage accumulation in the interstitium was completely abrogated and immune activation of the interstitial T cell infiltrate was prevented. This study demonstrates that IL-1 plays a key role in the pathogenesis of anti-GBM glomerulonephritis, and blocking its effects may provide a novel therapeutic approach to the treatment of human progressive glomerulonephritis. More... »

PAGES

479-485

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ki.1993.70

DOI

http://dx.doi.org/10.1038/ki.1993.70

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1046456222

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/8441245


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