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Rheumatology Advance Access originally published online on May 15, 2009
Rheumatology 2009 48(7):741-747; doi:10.1093/rheumatology/kep089
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© The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Serum amyloid A protein stimulates CCL20 production in rheumatoid synoviocytes

Kiyoshi Migita1, Tomohiro Koga1, Takafumi Torigoshi1, Yumi Maeda1, Taichiro Miyashita1, Yasumori Izumi1, Yoshihiro Aiba1, Atsumasa Komori1, Minoru Nakamura1, Satoru Motokawa1 and Hiromi Ishibashi1

1Department of Rheumatology, Clinical Research Center, NHO Nagasaki Medical Center, Omura, Japan.

Correspondence to: Kiyoshi Migita, Department of Rheumatology, Clinical Research Center, NHO Nagasaki Medical Center, Kubara 2-1001-1, Omura 856-8652, Japan. E-mail: migita{at}nmc.hosp.go.jp


  Abstract

Objective. Although serum amyloid A (SAA) has been used as a marker of inflammation, its role in leucocyte recruitment and angiogenesis has not been well established in RA. CCL20 is a chemokine involved in the migration of CCR6-expressing Th17 cells. To study the contribution of SAA to the recruitment of Th17 cells, we investigated the effects of SAA on CCL20 production by RA synoviotytes.

Methods. Synoviocytes isolated from RA patients were stimulated with recombinant SAA and cellular supernatants were analysed by CCL20-specific ELISA. CCL-20 mRNA expression was analysed by RT–PCR.

Results. SAA is a most potent inducer of CCL20 secretion in RA synoviocytes compared with other inflammatory cytokines (IL-1β, TNF-{alpha} and IL-17A). SAA stimulation induced CCL20 mRNA expression in RA synoviocytes, which was not affected by polymyxin B pre-treatment. SAA-induced CCL20 production was down-regulated by NF-{kappa}B inhibition and partially by c-jun N-terminal kinase (JNK) inhibition. SAA-induced CCL20 production was also suppressed by dexamethasone or FK506.

Conclusion. These findings suggest that SAA may be implicated in the recruitment of lymphocytes, including CCR6-expressing Th17 cells, in RA synovium by up-regulating CCL20 production in synoviocytes.

KEY WORDS: CCL20, Chemokines, FK506, Rheumatoid arthritis, Serum amyloid A, Synoviocytes, Th17 cells

Submitted 30 July 2008; revised version accepted 19 March 2009.
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