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Atherosclerosis. 2007 Feb;190(2):271-81. Epub 2006 Apr 18.

Infection with a periodontal pathogen increases mononuclear cell adhesion to human aortic endothelial cells.

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  • 1Division of Surgical Science, Department of Surgery, College of Physicians & Surgeons, Columbia University, New York, NY 10032, USA.



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.


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.


These data demonstrate that live invasive P. gingivalis 381 elicits a pro-atherogenic response in HAEC.

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