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Clues to Pathogenesis of Spondyloarthropathy Derived from Synovial Fluid Mononuclear Cell Gene Expression Profiles
JIERUO GU, MARKUS RIHL, ELISABETH MÄRKER-HERMANN, DOMINIQUE BAETEN, JENS G. KUIPERS, YEONG WOOK SONG, WALTER P. MAKSYMOWYCH, RUBEN BURGOS-VARGAS, ERIC M. VEYS, FILIP De KEYSER, HELMUTH DEISTER, MOMIAO XIONG, FENG HUANG, WEN CHAN TSAI, and DAVID TAK YAN YU
ABSTRACT.
Methods. Gene expression profiles were generated by microarray screening of SFMC of 5 patients with SpA, 5 patients with rheumatoid arthritis (RA), and peripheral blood mononuclear cells (PBMC) of 6 controls. Results were validated by reverse transcription polymerase chain reaction using samples from a larger panel of subjects. Results. The repertoires of proinflammatory cytokines/chemokines expressed by SpA and RA SFMC were very similar: monocyte chemotractant protein 1 (MCP-1), interleukin 8 (IL-8), IL-1ß, endothelial-monocyte activating polypeptide II, interferon-g, and tumor necrosis factor-a. MCP-1 was highly expressed in SpA SFMC. There was enhanced expression of immunoglobulin heavy chain binding protein (BiP) in SpA, which is compatible with the UPR hypothesis. BiP was most highly expressed in the adherent fraction of SpA SFMC. Conclusion. Previous data postulating UPR in SpA are based on in vitro experiments with transfected cell lines. Our patient derived data suggest that it also occurs in vivo in the macrophages of SpA joints. (J Rheumatol 2002;29:2159-64) Key Indexing Terms:
SPONDYLOARTHROPATHY
From the University of California Los Angeles, Los Angeles, CA, and the Human Genetics Center, University of Texas at Houston, Houston, TX, USA; the University of Mainz, Mainz, and the Hannover Medical School, Hannover, Germany; the University of Ghent, Ghent, Belgium; Seoul National University, Seoul, Korea; the University of Alberta, Edmonton, Canada; the Hospital General de Mexico, Universidad Nacional Autonoma de Mexico, Mexico City, Mexico; the Chinese PLA Hospital, Beijing, China; and Kaohsiung Medical University, Kaohsiung, Taiwan. Supported in part by a concerted action grant (GOA) of Ghent University; DFG Ku1182/1-3; the Alberta Heritage Foundation for Medical Research and the Canadian Institutes of Health; NIH grants GM56515 and HL5448; research grant 30025041 in China; and the Nora Eccles Treadwell Foundation at UCLA. J. Gu, MD, Postdoctoral Fellow; M. Rihl, MD, Postdoctoral Fellow; D.T.Y. Yu, MD, Professor of Medicine, University of California Los Angeles; E. Märker-Hermann, MD, Professor of Medicine; H. Deister, MD, Postdoctoral Fellow, University of Mainz; D. Baeten, MD, PhD, Rheumatology Fellow; E.M. Veys, MD, PhD, Professor of Medicine; F. De Keyser, MD, PhD, Professor of Medicine, University of Ghent; J.G. Kuipers, MD, Registrar and Lecturer, Hannover Medical School; Y.W. Song, MD, Professor of Medicine, Seoul National University; W.P. Maksymowych, MD, FRCP, Associate Professor of Medicine, University of Alberta; R. Burgos-Vargas, MD, Professor of Medicine, Hospital General de Mexico, Universidad Nacional Autonoma de Mexico; M. Xiong, PhD, Assistant Professor, Human Genetics Center, University of Texas at Houston; F. Huang, MD, Chinese PLA Hospital; W.C. Tsai, MD, Assistant Professor of Medicine, Kaohsiung Medical University. Address reprint requests to Dr. D. Yu, Rheumatology Division, 35-40 Rehabilitation Center, UCLA, 1000 Veteran Ave., Los Angeles, CA 90095-167022, USA. E-mail: DTYYU@ucla.edu Submitted September 6, 2001; revision accepted April 4, 2002. |