Disaccharide derived from chondroitin sulfate A suppressed CpG-induced IL-6 secretion in macrophage-like J774.1 cells

被引：9

作者：

Jin, Miao ^{[1
]}

Iwamoto, Taku ^{[1
]}

Yamada, Kiyoshi ^{[2
]}

Satsu, Hideo ^{[1
]}

Totsuka, Mamoru ^{[1
]}

Shimizu, Makoto ^{[1
]}

机构：

[1] Univ Tokyo, Dept Appl Biol Chem, Grad Sch Agr & Life Sci, Bunkyo Ku, Tokyo 1138657, Japan

[2] Nihon Univ, Sch Dent, Dept Microbiol, Chiyoda Ku, Tokyo 1018310, Japan

来源：

CYTOKINE | 2010年 / 51卷 / 01期

关键词：

Chondroitin sulfate A; Disaccharide; IL-6; CpG; J774.1; TOLL-LIKE RECEPTORS; COLLAGEN-INDUCED ARTHRITIS; TUMOR-NECROSIS-FACTOR; LEUCINE-RICH REPEATS; BACTERIAL-DNA; AUTOIMMUNE ENCEPHALOMYELITIS; IL-6-DEFICIENT MICE; KNEE OSTEOARTHRITIS; MANNOSE RECEPTOR; T-CELL;

D O I：

10.1016/j.cyto.2010.03.002

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Interleukin (IL)-6 secretion from macrophage cells is known to be induced by toll-like receptor (TLR) 9 ligands, CpG (microbial DNA sequences containing unmethylated CpG dinucleotides). We have found, using macrophage-like J774.1 cells, that this induction was dramatically suppressed by a disaccharide derived from chondroitin sulfate A (Di-4S), but not by chondroitin sulfate A (CS-A) itself. The suppression of IL-6 secretion by Di-4S occurred at protein and mRNA expression levels. Di-4S inhibited the degradation of interleukin-1 receptor-associated kinase 1 (IRAK1) in the signaling pathway mediated by myeloid differentiation primary response gene (88) (MyD88) when stimulated by TLR9 activation. In addition to suppressing IRAK1 activation, interference with CpG-TLR9 interaction by Di-4S is also suggested to be one of the mechanisms. Oligosaccharides derived from chondroitin sulfates would be effective suppressing agents for the TLR9-mediated inflammation reaction. (C) 2010 Elsevier Ltd. All rights reserved.

引用

页码：53 / 59

页数：7

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