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Rheumatology Advance Access originally published online on June 27, 2003
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Rheumatology 2003; 42: 1390-1397
© 2003 British Society for Rheumatology

Activated leucocytes express and secrete macrophage inflammatory protein-1{alpha} upon interaction with synovial fibroblasts of rheumatoid arthritis via a ß2-integrin/ICAM-1 mechanism

M. Hanyuda, T. Kasama, T. Isozaki, M. M. Matsunawa, N. Yajima, H. Miyaoka1, H. Uchida2, Y. Kameoka3, H. Ide and M. Adachi

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

Correspondence to: T. Kasama, Division of Rheumatology and Clinical Immunology, First Department of Internal Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8666, Japan. E-mail: tkasama{at}med.showa-u.ac.jp

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 ß2-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, ß2-integrin, Intercellular adhesion molecule 1, Monocytes, polymorphonuclear neutrophils, Synovitis, Chemokines.


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