pubmed-article:7516723 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7516723 | lifeskim:mentions | umls-concept:C0017658 | lld:lifeskim |
pubmed-article:7516723 | lifeskim:mentions | umls-concept:C0063695 | lld:lifeskim |
pubmed-article:7516723 | lifeskim:mentions | umls-concept:C1704264 | lld:lifeskim |
pubmed-article:7516723 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
pubmed-article:7516723 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:7516723 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
pubmed-article:7516723 | lifeskim:mentions | umls-concept:C1517004 | lld:lifeskim |
pubmed-article:7516723 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:7516723 | lifeskim:mentions | umls-concept:C0301625 | lld:lifeskim |
pubmed-article:7516723 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:7516723 | pubmed:issue | 9 | lld:pubmed |
pubmed-article:7516723 | pubmed:dateCreated | 1994-7-27 | lld:pubmed |
pubmed-article:7516723 | pubmed:abstractText | Interleukin-1 is a proinflammatory cytokine produced in glomerulonephritis. Blocking the action of interleukin-1 by the administration of the interleukin-1 receptor antagonist (IL-1ra) has been shown to prevent renal function impairment, reduce glomerular injury, inhibit leukocyte infiltration, and suppress tubulointerstitial damage in experimental antiglomerular basement membrane disease. A key mechanism in the entry of leukocytes into the kidney is the interaction between the interleukin-1 inducible intercellular adhesion molecule-1 (ICAM-1; CD54) and lymphocyte function-associated antigen-1 (CD11a/CD18). Therefore, this study investigated whether the inhibition of this mechanism was the means by which IL-1ra suppressed leukocyte infiltration in rat accelerated antiglomerular basement membrane glomerulonephritis. Disease was induced in two groups of six rats; animals were treated by constant sc infusion of recombinant human IL-1ra or saline from the initiation of disease until being euthanized 14 days later. In saline-treated animals, there was marked up-regulation of ICAM-1 in the glomerulus and interstitium, In which was associated with leukocyte infiltration. In particular, focal accumulation of CD11a+ and CD18+ cells was apparent in areas of tubulointerstitial damage exhibiting intense ICAM-1 expression. IL-1ra treatment partially reduced glomerular ICAM-1 expression and leukocyte infiltration. However, IL-1ra treatment resulted in a dramatic inhibition of interstitial ICAM-1 expression, interstitial leukocyte infiltration, and tubulointerstitial damage. In conclusion, this study has shown that interleukin-1 is a major inducer of ICAM-1 expression within the renal tubulo-interstitium--a process associated with focal leukocyte infiltration and tubulointerstitial damage.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
pubmed-article:7516723 | pubmed:language | eng | lld:pubmed |
pubmed-article:7516723 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7516723 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:7516723 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7516723 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7516723 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7516723 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7516723 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7516723 | pubmed:month | Mar | lld:pubmed |
pubmed-article:7516723 | pubmed:issn | 1046-6673 | lld:pubmed |
pubmed-article:7516723 | pubmed:author | pubmed-author:AtkinsR CRC | lld:pubmed |
pubmed-article:7516723 | pubmed:author | pubmed-author:HillP APA | lld:pubmed |
pubmed-article:7516723 | pubmed:author | pubmed-author:CHIT HTH | lld:pubmed |
pubmed-article:7516723 | pubmed:author | pubmed-author:VanniceJ LJL | lld:pubmed |
pubmed-article:7516723 | pubmed:author | pubmed-author:Nikolic-Pater... | lld:pubmed |
pubmed-article:7516723 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7516723 | pubmed:volume | 4 | lld:pubmed |
pubmed-article:7516723 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7516723 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7516723 | pubmed:pagination | 1695-700 | lld:pubmed |
pubmed-article:7516723 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
pubmed-article:7516723 | pubmed:meshHeading | pubmed-meshheading:7516723-... | lld:pubmed |
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pubmed-article:7516723 | pubmed:meshHeading | pubmed-meshheading:7516723-... | lld:pubmed |
pubmed-article:7516723 | pubmed:year | 1994 | lld:pubmed |
pubmed-article:7516723 | pubmed:articleTitle | Suppression of experimental glomerulonephritis by the interleukin-1 receptor antagonist: inhibition of intercellular adhesion molecule-1 expression. | lld:pubmed |
pubmed-article:7516723 | pubmed:affiliation | Department of Nephrology, Monash Medical Centre, Clayton, Victoria, Australia. | lld:pubmed |
pubmed-article:7516723 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:7516723 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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