Etanercept reduces the serum levels of interleukin-23 and macrophage inflammatory protein-3 alpha in patients with rheumatoid arthritis

被引:57
作者
Kageyama, Yasunori [1 ]
Ichikawa, Tetsuya [1 ]
Nagafusa, Tetsuyuki [1 ]
Torikai, Eiji [1 ]
Shimazu, Masahiro [1 ]
Nagano, Akira [1 ]
机构
[1] Hamamatsu Univ Sch Med, Dept Orthopaed Surg, Hamamatsu, Shizuoka 4313125, Japan
关键词
etanercept; rheumatoid arthritis; IL-23; MIP-3; alpha;
D O I
10.1007/s00296-007-0388-4
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The purpose of this study was to analyze the effect of the soluble TNF-alpha receptor etanercept on the serum levels of IL-16, IL-17, IL-23, and macrophage inflammatory protein-3 alpha (MIP-3 alpha) in rheumatoid arthritis (RA) patients. Twenty-two patients with RA were administered etanercept once or twice a week for more than 6 months, and we evaluated clinical and laboratory parameters and serum levels of IL-16, IL-17, IL-23, and MIP-3 alpha at the baseline and at 3 and 6 months. Additionally, the production of IL-23 and MIP-3 alpha of cultured synovial cells stimulated with TNF-alpha from RA patients was determined by ELISA. We also used ELISA kits to determine synovial fluid (SF) levels of IL-17, IL-23, and MIP-3 alpha in patients with RA, osteoarthritis (OA), pseudogouty arthritis (PGA), and gouty arthritis (GA). A significant decrease in serum levels of IL-23 and MIP-3 alpha was observed at 3 and 6 months after initial treatment of etanercept. TNF-alpha induced MIP-3 alpha but not IL-23 production in cultured synovial cells from RA patients. SF levels of IL-17, IL-23, and MIP-3 alpha in RA patients showed significantly higher levels than those of OA, PGA, and GA patients. This study demonstrated that the reduction of IL-23 and MIP-3 alpha production in RA patients was a newly determined function of etanercept
引用
收藏
页码:137 / 143
页数:7
相关论文
共 50 条
[31]   CCL20 chemokine induces both osteoblast proliferation and osteoclast differentiation: Increased levels of CCL20 are expressed in subchondral bone tissue of rheumatoid arthritis patients [J].
Lisignoli, Gina ;
Piacentini, Anna ;
Cristino, Sandra ;
Grassi, Francesco ;
Cavallo, Carola ;
Cattini, Luca ;
Tonnarelli, Beatrice ;
Manferdini, Cristina ;
Facchini, Andrea .
JOURNAL OF CELLULAR PHYSIOLOGY, 2007, 210 (03) :798-806
[32]   A phase II study of etanercept (enbrel), a tumor necrosis factor α inhibitor in patients with metastatic breast cancer [J].
Madhusudan, S ;
Foster, M ;
Muthuramalingam, SR ;
Braybrooke, JP ;
Wilner, S ;
Kaur, K ;
Han, C ;
Hoare, S ;
Balkwill, F ;
Talbot, DC ;
Ganesan, TS ;
Harris, AL .
CLINICAL CANCER RESEARCH, 2004, 10 (19) :6528-6534
[33]   Anti-cytokine therapy for rheumatoid arthritis [J].
Maini, RN ;
Taylor, PC .
ANNUAL REVIEW OF MEDICINE, 2000, 51 :207-229
[34]   Selective recruitment of CCR6-expressing cells by increased production of MIP-3α in rheumatoid arthritis [J].
Matsui, T ;
Akahoshi, T ;
Namai, R ;
Hashimoto, A ;
Kurihara, Y ;
Rana, M ;
Nishimura, A ;
Endo, H ;
Kitasato, H ;
Kawai, S ;
Takagishi, K ;
Kondo, H .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2001, 125 (01) :155-161
[35]   Divergent pro- and Antiinflammatory roles for IL-23 and IL-12 in joint autoimmune inflammation [J].
Murphy, CA ;
Langrish, CL ;
Chen, Y ;
Blumenschein, C ;
McClanahan, T ;
Kastelein, RA ;
Sedgwick, JD ;
Cua, DJ .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 198 (12) :1951-1957
[36]  
Paleolog EM, 1998, ARTHRITIS RHEUM, V41, P1258, DOI 10.1002/1529-0131(199807)41:7<1258::AID-ART17>3.0.CO
[37]  
2-1
[38]   Anti-tumour necrosis factor (TNF) α treatment of rheumatoid arthritis (infliximab) selectively down regulates the production of interleukin (IL) 18 but not of IL12 and IL13 [J].
Pittoni, V ;
Bombardieri, M ;
Spinelli, FR ;
Scrivo, R ;
Alessandri, C ;
Conti, F ;
Spadaro, A ;
Valesini, G .
ANNALS OF THE RHEUMATIC DISEASES, 2002, 61 (08) :723-725
[39]   Cloning and characterization of a specific receptor for the novel CC chemokine MIP-3 alpha from lung dendritic cells [J].
Power, CA ;
Church, DJ ;
Meyer, A ;
Alouani, S ;
Proudfoot, AEI ;
ClarkLewis, I ;
Sozzani, S ;
Mantovani, A ;
Wells, TNC .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 186 (06) :825-835
[40]   NF-κB inhibits TNF-induced accumulation of ROS that mediate prolonged MAPK activation and necrotic cell death [J].
Sakon, S ;
Xue, X ;
Takekawa, M ;
Sasazuki, T ;
Okazaki, T ;
Kojima, Y ;
Piao, JH ;
Yagita, H ;
Okumura, K ;
Doi, T ;
Nakano, H .
EMBO JOURNAL, 2003, 22 (15) :3898-3909