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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1993-4-1
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pubmed:abstractText |
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.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Complement C3,
http://linkedlifedata.com/resource/pubmed/chemical/IL1RN protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin 1 Receptor Antagonist...,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Sialoglycoproteins
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0085-2538
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
43
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
479-85
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8441245-Animals,
pubmed-meshheading:8441245-Basement Membrane,
pubmed-meshheading:8441245-Complement C3,
pubmed-meshheading:8441245-Glomerulonephritis,
pubmed-meshheading:8441245-Immunoglobulin G,
pubmed-meshheading:8441245-Interleukin 1 Receptor Antagonist Protein,
pubmed-meshheading:8441245-Interleukin-1,
pubmed-meshheading:8441245-Kidney Glomerulus,
pubmed-meshheading:8441245-Leukocytes,
pubmed-meshheading:8441245-Male,
pubmed-meshheading:8441245-Rats,
pubmed-meshheading:8441245-Rats, Sprague-Dawley,
pubmed-meshheading:8441245-Receptors, Interleukin-1,
pubmed-meshheading:8441245-Sialoglycoproteins
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pubmed:year |
1993
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pubmed:articleTitle |
Suppression of experimental crescentic glomerulonephritis by the interleukin-1 receptor antagonist.
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pubmed:affiliation |
Department of Nephrology, Monash Medical Centre, Melbourne, Australia.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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