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High CCL18/PARC Expression in Articular Cartilage and Synovial Tissue of Patients with Rheumatoid Arthritis
SHIGEKI MOMOHARA, HIROSHI OKAMOTO, TAKUJI IWAMOTO, TAMAO MIZUMURA, KATSUNORI IKARI, YASUSHI KAWAGUCHI, MASAHIRO TAKEUCHI, NAOYUKI KAMATANI, and TAISUKE TOMATSU ABSTRACT. Objective. We studied the role of CCL18/pulmonary and activation-regulated chemokine (PARC) in rheumatoid arthritis (RA). Methods. Human cartilage tissues and synovial membranes were obtained from patients with RA and with osteoarthritis (OA). Sera samples were obtained from RA patients, OA patients, healthy controls, and patients with flu, and synovial fluid (SF) from patients with RA and OA. Real-time PCR was performed with RNA from cartilage samples. Immunohistochemical analysis of CCL18/PARC was done with RA and OA cartilage and synovial tissue. Levels of CCL18/PARC in serum and SF were evaluated by ELISA. Results. CCL18/PARC mRNA was expressed at significantly higher levels in RA cartilage than in OA (p = 0.0001) and control (p < 0.0001) samples. CCL18/PARC mRNA expression was much higher in RA synovial membrane than OA samples (p = 0.0001). All RA cartilage and synovial tissue samples exhibited medium to strong staining for CCL18/PARC. Serum levels of CCL18/PARC were higher in RA patients (156.21 ± 125.73 ng/ml, n = 71) than in OA patients (64.54 ± 40.90 ng/ml, n = 12) and controls (28.04 ± 10.96 ng/ml, n = 20). Levels of CCL18/PARC in RA SF (275.20 ± 228.16 ng/ml, n = 15) were higher than in OA (33.13 ± 14.84 ng/ml, n = 6; p = 0.0198). CCL18/PARC levels correlated significantly with rheumatoid factor levels (r = 0.431, p = 0.0040), but not with matrix metalloproteinase-3, erythrocyte sedimentation rate, and C-reactive protein. Conclusion. CCL18/PARC was highly expressed in RA articular cartilage and synovial tissue compared with OA samples. Our data indicated that CCL18/PARC levels are not related to the conditions of generalized inflammation, but are related to the pathogenesis of RA. (J Rheumatol 2007;34:266–71) Key Indexing Terms:
RHEUMATOID ARTHRITIS From the Institute of Rheumatology, Tokyo Women's Medical University, Tokyo; and Institute for Drug Discovery, Yamanouchi Pharmaceutical Co., Ltd., Ibaraki, Japan. S. Momohara, MD, PhD; H. Okamoto, MD, PhD; T. Iwamoto, MD; T. Mizumura, MD; K. Ikari, MD, PhD; Y. Kawaguchi, MD, PhD, Institute of Rheumatology, Tokyo Women's Medical University; M. Takeuchi, PhD, Institute for Drug Discovery, Astellas Pharma Inc., N. Kamatani, MD, PhD; T. Tomatsu, MD, PhD, Institute of Rheumatology, Tokyo Women's Medical University. Address reprint requests to Dr. H. Okamoto, Institute of Rheumatology, Tokyo Women's Medical University, 10-22 Kawada-cho, Shinjuku-ku, Tokyo, 162-0054, Japan. E-mail: hokamoto@ior.twmu.ac.jp Accepted for publication October 13, 2006.
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