Porphyromonas gingivalis 67-kDa fimbriae induced cytokine production and osteoclast differentiation utilizing TLR2
Porphyromonas gingivalis 67-kDa fimbriae induced cytokine production and osteoclast differentiation utilizing TLR2
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DOI：
10.1016/s0378-1097(03)00788-2
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发表时间：
2003-12-05
影响因子：
2.1
通讯作者：
Umemoto, T
中科院分区：
文献类型：
--
作者：
Hiramine, H;Watanabe, K;Umemoto, T
牙龈卟啉单胞菌是引起成人牙周炎的主要病原菌，其细胞表面有两种截然不同的菌毛。主要菌毛;其由牙龈卟啉单胞菌ATCC 33277的41-kDa菌毛蛋白组成，已知其在鼠腹膜巨噬细胞中诱导炎性细胞因子的产生。在这项研究中，我们研究了牙龈卟啉单胞菌的次要菌毛，由67 kDa的菌毛蛋白，对小鼠腹腔巨噬细胞的细胞因子的产生和诱导破骨细胞分化的能力的影响。用牙龈卟啉单胞菌67-kDa次要菌毛刺激小鼠腹腔巨噬细胞24 h，然后用酶联免疫吸附试验（ELISA）测定白细胞介素（IL）-1 β、肿瘤坏死因子（TNF）-α和IL-6的水平。为了评估破骨细胞分化，将小鼠破骨细胞前体置于牙本质切片上，并与或不与牙龈卟啉单胞菌67-kDa小菌毛一起培养7天。牙龈卟啉单胞菌67-kDa次要菌毛明显诱导小鼠巨噬细胞产生IL-1 β、TNF-α和IL-6。此外，当破骨细胞前体与牙龈卟啉单胞菌67-kDa小菌毛孵育时，牙本质切片上的小凹形成显著延长。用抗Toll样受体2（TLR 2）抗体预处理显著抑制小鼠巨噬细胞中IL-1 β、TNF-α和IL-6的诱导（P < 0.05）以及用牙龈卟啉单胞菌67-kDa小菌毛刺激的破骨细胞前体细胞的成孔活性。这些结果表明，牙龈卟啉单胞菌67-kDa次要菌毛可能引起宿主炎症反应，并参与牙周组织的破坏。(C)2003年，欧洲微生物学会联合会。Elsevier B. V.出版，保留所有权利。
Porphyromonas gingivalis, a major etiological agent of adult periodontitis, has two distinctly different types of fimbriae on the cell surface. The major fimbriae; which consist of a 41-kDa fimbrillin of P. gingivalis ATCC 33277, have been known to induce inflammatory cytokine production in murine peritoneal macrophages. In this study, we examined the effects of the minor fimbriae of P. gingivalis, composed of a 67-kDa fimbrillin, on cytokine production in murine peritoneal macrophages and the ability to induce osteoclast differentiation. Murine peritoneal macrophages were stimulated with P. gingivalis 67-kDa minor fimbriae for 24 h, then the levels of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and IL-6 production were determined by enzyme-linked immunosorbent assay (ELISA). To estimate osteoclast differentiation, mouse osteoclast precursors were placed on dentine slices, and cultured with or without P. gingivalis 67-kDa minor fimbriae for 7 days. P. gingivalis 67-kDa minor fimbriae clearly induced IL-1beta, TNF-alpha and IL-6 production in mouse macrophages. Furthermore, pit formations on the dentine slices were significantly extended when the osteoclast precursors were incubated with P. gingivalis 67-kDa minor fimbriae. Pretreatment with anti-Toll-like receptor 2 (TLR2) antibody significantly inhibited IL-1beta, TNF-alpha and IL-6 induction (P < 0.05) in mouse macrophages and pit-forming activity of osteoclast precursor cells stimulated with P. gingivalis 67-kDa minor fimbriae. These results suggest that P. gingivalis 67-kDa minor fimbriae may provoke host inflammatory response and be involved in periodontal tissue breakdown. (C) 2003 Federation of European Microbiological Societies. Published by Elsevier B.V. All rights reserved.