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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.

Abstract

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.

[PubMed - indexed for MEDLINE]
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