Objective. Inflammation in MRL/lpr mice may involve dysfunctional leucocyte
-endothelial cell (EC) interactions. Previously, we have shown that interce
llular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (
VCAM-1) increase with age in a tumour necrosis factor alpha (TNF alpha)- an
d interleukin-1 (IL-1)-dependent manner. The object of this study was to de
termine the expression of E- and P-selectin.
Methods. Selectin expression was quantified in MRL/lpr mice and BALB/c cont
rols 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 sel
ectin inducibility, as a further inflammatory stimulus (intraperitoneal lip
opolysaccharide) resulted in up-regulation. Serum from older MRL/lpr did no
t induce selectin expression by EC in vitro.
Conclusion. The increase in E-selectin in the kidney may contribute to the
development of glomerulonephritis. However, the lack of systemic E- and P-s
electin expression may represent a protective mechanism which limits the in
teraction between leucocytes and the endothelium in the chronic inflammator
y context.