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© 1996 British Society for Rheumatology

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CHARACTERIZATION OF E-SELECTIN EXPRESSION, LEUCOCYTE TRAFFIC AND CLINICAL SEQUELAE IN URATE CRYSTAL-INDUCED INFLAMMATION: AN INSIGHT INTO GOUT

P. T. CHAPMAN, F. JAMAR*, A. A. HARRISON, J. B. SCHOFIELD{dagger}, A. M. PETERS*, R. M. BINNS{ddagger} and D. O. HASKARD

*Diagnostic Radiology, Royal Postgraduate Medical School, Hammersmith Hospital Du Cane Road, London W12 ONN
{dagger}Histopathology, Royal Postgraduate Medical School, Hammersmith Hospital Du Cane Road, London W12 ONN
{ddagger}Department of Immunology, The Babraham Institute Babraham, Cambridge CB2 4AT
Departments of Medicine (Rheumatology Unit), Royal Postgraduate Medical School, Hammersmith Hospital Du Cane Road, London W12 ONN

Correspondence to: Correspondence to: D. O. Haskard, Rheumatology Unit, Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, Du Cane Road, London W12 0NN.

The self-limiting response to urate crystals allows the exploration of events involved in both the onset and resolution of gout. Using i.v. injected radiolabelled anti-E-selectin monoclonal antibody 1.2B6 together with differentially radiolabelled neutrophils, mononuclear cells and albumin, we have characterized the expression of E-selectin in relation to leucocyte traffic, microvascular permeability and clinical sequelae following intracutaneous injection of monosodium urate crystals. We found that the inflammatory response in this model involved several distinct phases. First, E-selectin expression increased over 2–6 h in the context of increases in neutrophil and mononuclear cell accumulation, and albumin leakage. Secondly, leucocyte accumulation rapidly declined despite persisting E-selectin expression. Thirdly, E-selectin expression peaked at ~ 8 h and then fell despite an increase in clinically detectable erythema and induration. Lastly, these clinical manifestations of inflammation resolved despite the continued presence of urate crystals in the tissues. The further dissection of mechanisms regulating these phases will lead to a better understanding of events in both the pathogenesis and resolution of gout. Of broader significance, this inflammatory model may yield information about the protective events that underly resolution of inflammation, and provide insights into factors which determine chronicity.

KEY WORDS: Gout, Uric acid, E-selectin, Leucocyte migration


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