Osteoclast differentiation by human osteoblastic cell line SaOS-2 primed with bacterial lipid A
Osteoclast differentiation by human osteoblastic cell line SaOS-2 primed with bacterial lipid A
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DOI：
10.1016/s0928-8244(03)00111-1
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发表时间：
2003-08-18
影响因子：
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通讯作者：
Ogawa, T
中科院分区：
文献类型：
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作者：
Asai, Y;Hirokawa, Y;Ogawa, T
我们研究了人成骨细胞系SaOS-2在人外周血单个核细胞（PBMC）破骨细胞分化过程中对细菌脂质A（脂多糖的生物活性中心）的反应。SaOS-2细胞表达Toll样受体（TLR）4、MD-2的mRNA。CD 14和髓样分化因子88，而它们不能表达TLR 2的mRNA。大肠杆菌型合成脂质A（化合物506）诱导SaOS-2细胞中细胞因子mRNA表达和核因子（NF）-kappaB活化。化合物506还增加NF-κ B配体的受体激活剂的表达。此外，用化合物506致敏的细胞增强PBMC向成骨细胞的分化，并且该作用被抗TLR 4单克隆抗体抑制。这些结果表明，TLR信号级联在成骨细胞参与调节破骨细胞的功能。(C)2003年，欧洲微生物学会联合会。由Elsevier Science B. V.出版，版权所有。
We examined the responses of human osteoblastic cell line SaOS-2 to bacterial lipid A, a bioactive center of lipopolysaccharide, during osteoclast differentiation of human peripheral blood mononuclear cells (PBMC). SaOS-2 cells expressed mRNA for Toll-like receptor (TLR) 4, MD-2. CD14, and myeloid differentiation factor 88, whereas they failed to express mRNA for TLR2. Escherichia coli-type synthetic lipid A (compound 506) induced cytokine mRNA expression and nuclear factor (NF)-kappaB activation in SaOS-2 cells. Compound 506 also increased the expression of receptor activator of NF-kappaB ligand. Further, cells primed with compound 506 augmented the differentiation of PBMC into osteoclastic cells, and the effect was inhibited by anti-TLR4 monoclonal antibody. These findings suggest that the TLR signaling cascade in osteoblastic cells is involved in regulating the function of osteoclastogenesis. (C) 2003 Federation of European Microbiological Societies. Published by Elsevier Science B.V. All rights reserved.