Extended exposure of lipopolysaccharide fraction from Porphyromonas gingivalis facilitates mononuclear cell adhesion to vascular endothelium via Toll-like receptor-2 dependent mechanism
Extended exposure of lipopolysaccharide fraction from Porphyromonas gingivalis facilitates mononuclear cell adhesion to vascular endothelium via Toll-like receptor-2 dependent mechanism
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DOI：
10.1016/j.atherosclerosis.2007.01.039
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发表时间：
2008-01-01
期刊：
影响因子：
5.3
通讯作者：
Iwai, Takehisa
中科院分区：
文献类型：
--
作者：
Nakamura, Naokazu;Yoshida, Masayuki;Iwai, Takehisa
某些感染性病原体有助于动脉粥样硬化形成。事实上，牙周病原体，如牙龈卟啉单胞菌（P.g.）和冠心病已经被证实。我们研究了P.G.单核细胞-内皮细胞相互作用。从厌氧条件下培养的Pg.中提取脂多糖（LPS）级分，并与从大肠杆菌（E. coli）菌株（JM 109）。人脐静脉内皮细胞（HUVEC）在Pg. - LPS组分或E. coli-LPS组分，并在流动下进行单核细胞粘附测定。单核细胞与经Pg. -处理的HUVECs的粘附LPS在培养24 h后达到高峰，而E. coli-LPS部分在孵育4小时后最大化。荧光免疫结合试验显示，Pg. - LPS组分显著上调HUVECs ICAM-1和VCAM-1表达。抗ICAM-1和Toll样受体（TLR）-2抗体，而不是TLR-4，减弱Pg。LPS组分促进单核细胞与HUVECs的粘附。总之，这些结果表明，慢性前列腺素感染可能通过持续上调ICAM-1和VCAM-1促进单核细胞募集到血管内皮。我们的研究结果提供了新的证据表明TLR-2通路可能通过介导Pg. LPS信号转导。(C)2007爱思唯尔爱尔兰有限公司保留所有权利。
Certain infectious pathogens contribute to atherogenesis. Indeed, the strong relationship between periodontal pathogens, such as Porphyromonas gingivalis (P.g.) and coronary heart disease has been demonstrated. We investigated the potential role of P.g. in monocyte-endothelial interaction. Lipopolysaccharide (LPS) fraction was extracted from Pg. cultured under anaerobic conditions and compared to that obtained from an Escherichia coli (E. coli) strain (JM109). Human umbilical vein endothelial cells (HUVECs) were incubated in the presence of Pg.-LPS fraction or E. coli-LPS fraction for various periods and mononuclear cell adhesion assays were conducted under flow. The adhesion of mononuclear cells to HUVECs treated with Pg.-LPS fraction peaked after 24 h of incubation, whereas those treated with E. coli-LPS fraction maximized after 4 h of incubation. A fluorescent immunobinding assay revealed that Pg.-LPS fraction significantly upregulated ICAM-1 and VCAM-1 in HUVECs. Antibodies against ICAM-1 and Toll-like receptor (TLR)-2, but not TLR-4, attenuated Pg.-LPS fraction-facilitated mononuclear cell adhesion to HUVECs. In conclusion, these results suggest that chronic Pg. infection may facilitate monocyte recruitment to vascular endothelium through sustained upregulation of ICAM-1 and VCAM-1. Our findings provide new evidence that the TLR-2 pathway may contribute to atherogenesis by mediating Pg.-LPS signal transduction. (C) 2007 Elsevier Ireland Ltd. All rights reserved.