Journal
ATHEROSCLEROSIS
Volume 190, Issue 2, Pages 271-281Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.atherosclerosis.2006.03.018
Keywords
periodontitis; atherosclerosis; infection; Porphyromonas gingivalis; endothelial cell
Funding
- NIDCR NIH HHS [DE14575, DE14490] Funding Source: Medline
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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 gingivatis 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. R 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 inononuclear 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. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
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