Linked Life Data

10491002

Source:http://linkedlifedata.com/resource/pubmed/id/10491002

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1999-10-21
pubmed:abstractText
Dysfunctional leukocyte-endothelial interactions are thought to play a key role in systemic lupus erythematosus pathogenesis. We questioned the importance of TNF-alpha and IL-1 for endothelial activation in MRL/lpr lupus-prone mice. Endothelial ICAM-1 and VCAM-1 expression increased significantly with disease evolution in kidney, heart, and brain, as shown by i.v. injected radiolabeled Ab uptake. Lung endothelial VCAM-1 also increased, while lung endothelial ICAM-1 did not rise above a high basal level. Immunoassays showed a significantly raised circulating level of TNF-alpha by 14 wk, with levels of circulating IL-1alpha and IL-1beta being additionally raised by 20 wk. With 14-wk-old MRL/lpr, anti-TNF-alpha antiserum inhibited expression of ICAM-1 and VCAM-1 by endothelial cells cultured with sera in vitro, and uptake of anti-ICAM-1 and anti-VCAM-1 mAb in lung, kidney, brain, and heart in vivo. In contrast, both anti-TNF-alpha and anti-IL-1 antisera were required for maximal inhibition in vitro and in vivo at 20 wk. These data indicate that TNF-alpha is largely responsible for the early up-regulation of endothelial ICAM-1 and VCAM-1, but that IL-1 enhances expression in late disease. Our observations provide novel insights of possible relevance to understanding endothelial activation in systemic lupus erythematosus, and highlight an approach that can be extended to dissecting other chronic inflammatory diseases.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
163
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3993-4000
pubmed:dateRevised
2010-8-25
pubmed:meshHeading
pubmed-meshheading:10491002-Animals, pubmed-meshheading:10491002-Brain, pubmed-meshheading:10491002-Cytokines, pubmed-meshheading:10491002-Endothelium, Vascular, pubmed-meshheading:10491002-Female, pubmed-meshheading:10491002-Immune Sera, pubmed-meshheading:10491002-Injections, Intraperitoneal, pubmed-meshheading:10491002-Intercellular Adhesion Molecule-1, pubmed-meshheading:10491002-Interleukin-1, pubmed-meshheading:10491002-Kidney, pubmed-meshheading:10491002-Lung, pubmed-meshheading:10491002-Lupus Nephritis, pubmed-meshheading:10491002-Mice, pubmed-meshheading:10491002-Mice, Inbred BALB C, pubmed-meshheading:10491002-Mice, Inbred MRL lpr, pubmed-meshheading:10491002-Myocardium, pubmed-meshheading:10491002-Tumor Necrosis Factor-alpha, pubmed-meshheading:10491002-Vascular Cell Adhesion Molecule-1
pubmed:year
1999
pubmed:articleTitle
TNF-alpha and IL-1 sequentially induce endothelial ICAM-1 and VCAM-1 expression in MRL/lpr lupus-prone mice.
pubmed:affiliation
British Heart Foundation Cardiovascular Medicine Unit, National Heart and Lung Institute, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't