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and IL-1 Sequentially Induce Endothelial ICAM-1 and VCAM-1 Expression in MRL/lpr Lupus-Prone Mice1
British Heart Foundation Cardiovascular Medicine Unit, National Heart and Lung Institute, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom
Dysfunctional leukocyte-endothelial interactions are thought to
play a key role in systemic lupus erythematosus pathogenesis. We
questioned the importance of TNF-
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-
by 14 wk, with levels of circulating IL-1 and IL-1ß being
additionally raised by 20 wk. With 14-wk-old MRL/lpr,
anti-TNF- 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- and anti-IL-1
antisera were required for maximal inhibition in vitro and in vivo at
20 wk. These data indicate that TNF- 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.
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