Biological activities of Bacteroides forsythus lipoproteins and their possible pathological roles in periodontal disease
Biological activities of Bacteroides forsythus lipoproteins and their possible pathological roles in periodontal disease
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DOI：
10.1128/iai.72.3.1318-1325.2004
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发表时间：
2004-03-01
影响因子：
3.1
通讯作者：
Shibata, K
中科院分区：
文献类型：
--
作者：
Hasebe, A;Yoshimura, A;Shibata, K
拟杆菌是一种革兰氏阴性、厌氧、梭形细菌，被认为是牙周病的病原体。由B制备的脂蛋白级分。经Triton X-114相分离（BfLP）的人牙龈成纤维细胞和人单核细胞系THP-1激活的人牙龈成纤维细胞诱导白细胞介素-6和肿瘤坏死因子α的产生。发现BfLP能够诱导人牙龈成纤维细胞和THP-1细胞中的核因子-κ B易位。通过使用Toll样受体基因转染的中国仓鼠卵巢K1细胞连同核因子-κ B依赖性CD 25报告质粒，发现BfLP的信号传导由Toll样受体2介导，而不是由CD 14或Toll样受体4介导。BfLP在人牙龈成纤维细胞、KB细胞（口腔上皮细胞系）、HL-60细胞（人髓性白血病细胞系）和THP-1细胞中诱导凋亡性细胞死亡，但在MOLT 4细胞（T细胞白血病细胞系）中不诱导。半胱天冬酶-8，一个引发凋亡的半胱天冬酶，被发现在这些细胞中被激活，响应于BfLP刺激。因此，这项研究表明，BfLP在口腔感染，特别是牙周病，通过诱导细胞活化或凋亡发挥一定的病因作用。
Bacteroides forsythus is a gram-negative, anaerobic, fusiform bacterium and is considered to be an etiological agent in periodontal disease. A lipoprotein fraction prepared from B. forsythus cells by Triton X-114 phase separation (BfLP) activated human gingival fibroblasts and a human monocytic cell line, THP-1, to induce interleukin-6 production and tumor necrosis factor alpha production. BfLP was found to be capable of inducing nuclear factor-kappaB translocation in human gingival fibroblasts and THP-1 cells. By using Chinese hamster ovary K1 cells transfected with Toll-like receptor genes together with a nuclear factor-kappaB-dependent CD25 reporter plasmid, it was found that signaling by BfLP was mediated by Toll-like receptor 2 but not by CD14 or Toll-like receptor 4. BfLP induced apoptotic cell death in human gingival fibroblasts, KB cells (an oral epithelial cell line), HL-60 cells (a human myeloid leukemia cell line), and THP-1 cells but not in MOLT4 cells (a T-cell leukemia cell line). Caspase-8, an initiator caspase in apoptosis, was found to be activated in these cells in response to BfLP stimulation. Thus, this study suggested that BfLP plays some etiological roles in oral infections, especially periodontal disease, by induction of cell activation or apoptosis.