Serum amyloid A protein stimulates CCL20 production in rheumatoid synoviocytes

被引：25

作者：

Migita, Kiyoshi ^{[1
]}

Koga, Tomohiro ^{[1
]}

Torigoshi, Takafumi ^{[1
]}

Maeda, Yumi ^{[1
]}

Miyashita, Taichiro ^{[1
]}

Izumi, Yasumori ^{[1
]}

Aiba, Yoshihiro ^{[1
]}

Komori, Atsumasa ^{[1
]}

Nakamura, Minoru ^{[1
]}

Motokawa, Satoru ^{[1
]}

Ishibashi, Hiromi ^{[1
]}

机构：

[1] NHO Nagasaki Med Ctr, Dept Rheumatol, Clin Res Ctr, Omura 8568652, Japan

来源：

RHEUMATOLOGY | 2009年 / 48卷 / 07期

关键词：

CCL20; Chemokines; FK506; Rheumatoid arthritis; Serum amyloid A; Synoviocytes; Th17; cells; NF-KAPPA-B; SIGNAL-TRANSDUCTION PATHWAY; NECROSIS-FACTOR-ALPHA; ACUTE-PHASE; SYNOVIAL TISSUE; T-CELLS; GLUCOCORTICOID-RECEPTOR; CALCIUM MOBILIZATION; TNF-ALPHA; ARTHRITIS;

D O I：

10.1093/rheumatology/kep089

中图分类号：

R5 [内科学];

学科分类号：

100201 [内科学];

摘要：

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 RTPCR. Results. SAA is a most potent inducer of CCL20 secretion in RA synoviocytes compared with other inflammatory cytokines (IL-1, TNF- 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-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.

引用

页码：741 / 747

页数：7

共 39 条

[1]

Chemokine: Receptor structure, interactions, and antagonism [J].

Allen, Samantha J. ;

Crown, Susan E. ;

Handel, Tracy M. .

ANNUAL REVIEW OF IMMUNOLOGY, 2007, 25 :787-820

[2]

Phenotypic and functional features of human Th17 cells [J].

Annunziato, Francesco ;

Cosmi, Lorenzo ;

Santarlasci, Veronica ;

Maggi, Laura ;

Liotta, Francesco ;

Mazzinghi, Benedetta ;

Parente, Eliana ;

Fili, Lucia ;

Ferri, Simona ;

Frosali, Francesca ;

Giudici, Francesco ;

Romagnani, Paola ;

Parronchi, Paola ;

Tonelli, Francesco ;

Maggi, Enrico ;

Romagnani, Sergio .

JOURNAL OF EXPERIMENTAL MEDICINE, 2007, 204 (08) :1849-1861

[3]

BADOLATO R, 1995, J IMMUNOL, V155, P4004

[4]

Role of cytokines, acute-phase proteins, and chemokines in the progression of rheumatoid arthritis [J].

Badolato, R ;

Oppenheim, JJ .

SEMINARS IN ARTHRITIS AND RHEUMATISM, 1996, 26 (02) :526-538

[5]

TH-17 cells in the circle of immunity and autoimmunity [J].

Bettelli, Estelle ;

Oukka, Mohamed ;

Kuchroo, Vijay K. .

NATURE IMMUNOLOGY, 2007, 8 (04) :345-350

[6]

NEGATIVE CROSS-TALK BETWEEN RELA AND THE GLUCOCORTICOID RECEPTOR - A POSSIBLE MECHANISM FOR THE ANTIINFLAMMATORY ACTION OF GLUCOCORTICOIDS [J].

CALDENHOVEN, E ;

LIDEN, J ;

WISSINK, S ;

VANDESTOLPE, A ;

RAAIJMAKERS, J ;

KOENDERMAN, L ;

OKRET, S ;

GUSTAFSSON, JA ;

VANDERSAAG, PT .

MOLECULAR ENDOCRINOLOGY, 1995, 9 (04) :401-412

[7]

Enhancing effect of IL-1, IL-17, and TNF-α on macrophage inflammatory protein-3α production in rheumatoid arthritis:: Regulation by soluble receptors and Th2 cytokines [J].

Chabaud, M ;

Page, G ;

Miossec, P .

JOURNAL OF IMMUNOLOGY, 2001, 167 (10) :6015-6020

[8]

The interplay between the glucocorticoid receptor and nuclear factor-κB or activator protein-1:: Molecular mechanisms for gene repression [J].

De Bosscher, K ;

Vanden Berghe, W ;

Haegeman, G .

ENDOCRINE REVIEWS, 2003, 24 (04) :488-522

[9]

Feldmann M, 1999, RHEUMATOLOGY, V38, P3

[10]

A novel function of serum amyloid A:: A potent stimulus for the release of tumor necrosis factor-α, interleukin-1β, and interleukin-8 by human blood neutrophil [J].

Furlaneto, CJ ;

Campa, A .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2000, 268 (02) :405-408

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