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


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.


CONCLUSIONS
These data demonstrate that live invasive P. gingivalis 381 elicits a pro-atherogenic response in HAEC.
Roth
Georg A
GA
Division of Surgical Science, Department of Surgery, College of Physicians & Surgeons, Columbia University, New York, NY 10032, USA.
Moser
Bernhard
B
Roth-Walter
Franziska
F
Giacona
Mary Beth
MB
Harja
Evis
E
Papapanou
Panos N
PN
Schmidt
Ann Marie
AM
Lalla
Evanthia
E
D001011:Aorta / Q000382:microbiology / Q000502:physiology*; D001422:Bacterial Adhesion; D016866:Bacteroidaceae Infections; D002448:Cell Adhesion; D002478:Cells, Cultured; D016207:Cytokines / Q000032:analysis; D004730:Endothelium, Vascular / Q000382:microbiology* / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000382:microbiology; D010518:Periodontitis / Q000382:microbiology*; D016966:Porphyromonas gingivalis / Q000235:genetics / Q000472:pathogenicity
D016207:Cytokines