Limited endothelial E- and P-selectin expression in MRL/lpr lupus-prone mice.
OBJECTIVE
Inflammation in MRL/lpr mice may involve dysfunctional leucocyte-endothelial cell (EC) interactions. Previously, we have shown that intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) increase with age in a tumour necrosis factor alpha (TNF alpha)- and interleukin-1 (IL-1)-dependent manner. The object of this study was to determine the expression of E- and P-selectin.


METHODS
Selectin expression was quantified in MRL/lpr mice and BALB/c controls by intravenous injection of differentially radio-labelled antibodies.


RESULTS
E-selectin, but not P-selectin, was up-regulated in the kidneys of older mice. Neither was up-regulated elsewhere. There was no defect in selectin inducibility, as a further inflammatory stimulus (intraperitoneal lipopolysaccharide) resulted in up-regulation. Serum from older MRL/lpr did not induce selectin expression by EC in vitro.


CONCLUSIONS
The increase in E-selectin in the kidney may contribute to the development of glomerulonephritis. However, the lack of systemic E- and P-selectin expression may represent a protective mechanism which limits the interaction between leucocytes and the endothelium in the chronic inflammatory context.
Harari
O A
OA
BHF Cardiovascular Medicine Unit, National Heart & Lung Institute, Imperial College School of Medicine, Hammersmith Hospital, London W12 0NN, UK.
Marshall
D
D
McHale
J F
JF
Ahmed
S
S
Haskard
D O
DO
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D002460:Cell Line; D019040:E-Selectin / Q000096:biosynthesis*; D005260:Female; D007668:Kidney / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000633:toxicity; D008177:Lupus Vulgaris / Q000209:etiology*; D051379:Mice; D008807:Mice, Inbred BALB C; D019463:Mice, Inbred MRL lpr; D019007:P-Selectin / Q000096:biosynthesis*
D000911:Antibodies, Monoclonal; D019040:E-Selectin; D008070:Lipopolysaccharides; D019007:P-Selectin