Vol.23 No.1

Original Article

Serum amyloid A (SAA) induces pentraxin 3 (PTX3) production in rheumatoid synoviocytes

Authors

Kenshi Satomura1,2 , Takafumi Torigoshi1,2 , Tomohiro Koga4 , Yumi Maeda3 , Yasumori Izumi1 , Yuka Jiuchi3 , Taiichiro Miyashita1 , Satoshi Yamasaki4 , Atsushi Kawakami4 , Yoshihiro Aiba3 , Minoru Nakamura3 , Atsumasa Komori3, Junji Sato5, Hiromi Ishibashi3, Satoru Motokawa1,2, Kiyoshi Migita1,3

  • Department of Rheumatology, Nagasaki Medical Center, Omura, Nagasaki, 856-8562, Japan
  • Department of Orthopedic Surgery, Nagasaki Medical Center, Omura, Nagasaki, 856-8562, Japan
  • Clinical Research Center, NHO Nagasaki Medical Center, Kubara 2-1001-1, Omura, Nagasaki, 856-8562, Japan
  • Department of Rheumatology, Nagasaki University Hospital, Nagasaki, Japan
  • Research and Development Division, Eiken Chemical Co. Ltd, Nogi, Tochigi, Japan
Received:

17 August 2011

Accepted:

28 February 2012

Published online:

24 March 2012

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Abstract

Objective Pentraxin 3 (PTX3) is an acute-phase reactant that is involved in amplification of the inflammatory response and innate immunity. In the present study, we evaluated the relationship between PTX3 and serum amyloid A (SAA), another acute-phase reactant, in rheumatoid synoviocytes.
Methods PTX3 mRNA expression was examined by reverse transcription polymerase chain reaction, and PTX3 protein was measured by enzyme-linked immunosorbent assay.
Results SAA induced PTX3 mRNA and PTX3 protein expression in rheumatoid synoviocytes. SAA-induced PTX3 expression was attenuated when rheumatoid synoviocytes were nucleofected with N-formyl peptide receptor ligand-1 (FPRL-1)-specific siRNA, suggesting the involvement of FPRL-1. Furthermore, SAA-induced PTX3 expression was inhibited by NF-jB or mitogen-activated protein kinasespecific inhibitors. Neither soluble TNF receptor (etanercept) nor recombinant IL-1 receptor antagonist affected PTX3 production by SAA-stimulated synoviocytes, suggesting that SAA directly induces PTX3.
Conclusion Our data suggest that SAA plays a role in the proinflammatory and immune responses in rheumatoid synovium by inducing PTX3. We provide the first evidence that the acute-phase reactant SAA, which is produced systemically by hepatocytes, perpetuates the rheumatoid inflammatory processes by inducing another proinflammatory molecule, PTX3, locally in rheumatoid synovial tissues.

Key words

Pentraxin 3 - Rheumatoid arthritis - Serum amyloid A - Synoviocytes