感染牙周病原体可增加单核细胞对人主动脉内皮细胞的黏附。
Infection with a periodontal pathogen increases mononuclear cell adhesion to human aortic endothelial cells.
作者信息
Roth Georg A, Moser Bernhard, Roth-Walter Franziska, Giacona Mary Beth, Harja Evis, Papapanou Panos N, Schmidt Ann Marie, Lalla Evanthia
机构信息
Division of Surgical Science, Department of Surgery, College of Physicians & Surgeons, Columbia University, New York, NY 10032, USA.
出版信息
Atherosclerosis. 2007 Feb;190(2):271-81. doi: 10.1016/j.atherosclerosis.2006.03.018. Epub 2006 Apr 18.
BACKGROUND
As a link between periodontal infections and an increased risk for vascular disease has been demonstrated, we assessed the ability of the Gram-negative periodontal pathogen Porphyromonas gingivalis to modulate properties of endothelial cells linked to inflammation and proatherogenic pathways.
METHODS AND RESULTS
Primary human aortic endothelial cells (HAEC) were infected with either P. gingivalis strain 381 or its non-invasive fimbriae-deficient mutant, DPG3, and incubated with U-937 monocytes, or Jurkat T cells. P. gingivalis-infected HAEC demonstrated significantly increased adhesion of immune cells compared to non-infected cells or those infected with DPG3. Heat-killed bacteria had no effect on mononuclear cell adhesion and P. gingivalis LPS had only a minimal effect. P. gingivalis infection significantly increased HAEC expression of VCAM-1, ICAM-1 and E-selectin, and enhanced production of IL-6, IL-8 and MCP-1.
CONCLUSION
These data demonstrate that live invasive P. gingivalis 381 elicits a pro-atherogenic response in HAEC.
背景
由于牙周感染与血管疾病风险增加之间的联系已得到证实，我们评估了革兰氏阴性牙周病原体牙龈卟啉单胞菌调节与炎症和动脉粥样硬化发生途径相关的内皮细胞特性的能力。
方法与结果
用人牙龈卟啉单胞菌381株或其无侵袭性菌毛缺陷突变体DPG3感染原代人主动脉内皮细胞（HAEC），并与U-937单核细胞或Jurkat T细胞共同孵育。与未感染细胞或感染DPG3的细胞相比，感染牙龈卟啉单胞菌的HAEC显示免疫细胞的黏附显著增加。热灭活细菌对单核细胞黏附无影响，牙龈卟啉单胞菌脂多糖的影响极小。牙龈卟啉单胞菌感染显著增加了HAEC中VCAM-1、ICAM-1和E-选择素的表达，并增强了IL-6、IL-8和MCP-1的产生。
结论
这些数据表明，活的具有侵袭性的牙龈卟啉单胞菌381株在HAEC中引发了促动脉粥样硬化反应。
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