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Rheumatology Advance Access published online on June 27, 2003
Rheumatology, doi:10.1093/rheumatology/keg391
Rheumatology © British Society for Rheumatology 2003; all rights reserved
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© 2003 Rheumatology 42 © British Society for Rheumatology 2003; all rights reserved

Original Papers

Activated leucocytes express and secrete macrophage inflammatory protein-1{alpha} upon interaction with synovial fibroblasts of rheumatoid arthritis via a {beta}2-integrin/ICAM-1 mechanism

M. Hanyuda 1, T. Kasama 1*, T. Isozaki 1, M. M. Matsunawa 1, N. Yajima 1, H. Miyaoka 2, H. Uchida 3, Y. Kameoka 4, H. Ide 1, and M. Adachi 1

1 Division of Rheumatology and Clinical Immunology, First Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan
2 Department of Orthopedics, Showa University School of Medicine, Tokyo, Japan
3 Department of Orthopedics, Furukawabashi Hospital, Tokyo, Japan
4 Division of Genetic Resources, National Institute of Infectious Diseases, Tokyo, Japan

* Corresponding author. E-mail: tkasama{at}med.showa.

Received 11 February 2003 ; accepted 31 March 2003

Abstract

Objective. To examine the expression and regulation of chemotactic factor, macrophage inflammatory protein-1{alpha} (MIP-1{alpha}) by fibroblast-like synoviocytes (FLS), monocytes and polymorphonuclear neutrophils (PMN) isolated from the synovial fluid (SF) of rheumatoid arthritis (RA) patients.

Methods. Monocytes or PMN obtained from RA SF were co-cultured with unstimulated semiconfluent RA FLS. Culture supernatants were assayed for MIP-1{alpha} by enzyme-linked immunosorbent assay. The expression of MIP-1{alpha} mRNA and protein was also determined by Northern blot analyss and immunohistochemistry respectively.

Results. Interaction of activated leucocytes with FLS synergistically increased MIP-1{alpha} expression and secretion via a mechanism mediated by {beta}2-integrin/ intercellular adhesion molecule 1.

Conclusion. MIP-1{alpha} expression within inflamed joints appears to be regulated not only by inflammatory cytokines but also by the physical interaction of activated leucocytes and FLS, and plays a crucial role in the progression and maintenance of RA synovitis.

Key words: MIP-1{alpha}, Rheumatoid arthritis, Inflammatory cytokines, Fibroblast-like synoviocytes, {beta}2-integrin, Intercellular adhesion molecule 1, Monocytes, polymorphonuclear neutrophils, Synovitis, Chemokines.
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