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Rheumatology 2001; 40: 889-895
© 2001 British Society for Rheumatology

Original Papers

Limited endothelial E- and P-selectin expression in MRL/lpr lupus-prone mice

O. A. Harari, D. Marshall, J. F. McHale, S. Ahmed and D. O. Haskard

BHF Cardiovascular Medicine Unit, National Heart & Lung Institute, Imperial College School of Medicine, Hammersmith Hospital, London W12 0NN, UK

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.

Conclusion. 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.

KEY WORDS: Inflammation, Endothelium, Adhesion, E-selectin, P-selectin, MRL/lpr, Lupus, Glomerulonephritis.

Correspondence to: D. O. Haskard


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