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Rheumatology 2001; 40: 988-994
© 2001 British Society for Rheumatology

Original Papers

Expression of chemokines and matrix metalloproteinases in early rheumatoid arthritis

A. Katrib1,2, P. P. Tak3, J. V. Bertouch1, C. Cuello2, H. P. McNeil1,2, T. J. M. Smeets3, M. C. Kraan3 and P. P. Youssef2,4,

1 Rheumatology Unit, Prince of Wales Hospital,
2 Inflammation Research Unit, School of Pathology, University of New South Wales, Sydney, Australia,
3 Division of Clinical Immunology and Rheumatology, Academic Medical Centre, Amsterdam, The Netherlands and
4 The Combined Centre for the Rheumatic Diseases, Rachel Forster Hospital, Sydney, Australia

Objective. To compare macrophage infiltration and expression of chemokines and matrix metalloproteinases (MMPs) in synovial tissue between patients with early and long-standing rheumatoid arthritis (RA).

Methods. Knee synovial biopsies were taken from 22 patients with early (<1 yr) and 22 patients with long-standing (>5 yr) RA and immunostained with antibodies specific for CD68; macrophage inflammatory protein (MIP)-1{alpha} and monocyte chemoattractant protein (MCP)-1; MMP-1 and -3 and the tissue inhibitors of metalloproteinases (TIMP)-l and -2. Immunostaining was quantified using a colour video image analysis system.

Results. CD68+ macrophage infiltration and the expression of MIP-1{alpha}, MCP-1, MMP-1, MMP-3, TIMP-1, and TIMP-2 were observed in synovial tissue of patients with early RA. In long-standing RA, there was a further increase in CD68+ macrophage infiltration and MIP-1{alpha} expression in the synovial lining layer. CD68 expression correlated with MIP-1{alpha} (R=0.39, P=0.01), but not with MCP-1 expression.

Conclusion. Macrophage accumulation, and the expression of chemokines and MMPs in synovial tissue occur in early RA. Targeting chemokines which play a role in the migration of macrophages into the joints may be of therapeutic benefit in RA patients.

KEY WORDS: Rheumatoid arthritis, Chemokines, Matrix metalloproteinases, Tissue inhibitors of matrix metalloproteinases.

Correspondence to: P. P. Youssef, Inflammation Research Unit, School of Pathology, University of New South Wales, Sydney, 2052, Australia.


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