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

被引:104
作者
Roth, Georg A.
Moser, Bernhard
Roth-Walter, Franziska
Giacona, Mary Beth
Harja, Evis
Papapanou, Panos N.
Schmidt, Ann Marie
Lalla, Evanthia
机构
[1] Columbia Univ, Coll Dent Med, Div Peridont, Sect Oral & Diagnost Sci, New York, NY 10032 USA
[2] Columbia Univ, Coll Phys & Surg, Dept Surg, Div Surg Sci, New York, NY USA
[3] Mt Sinai Sch Med, Ctr Immunobiol, New York, NY USA
关键词
periodontitis; atherosclerosis; infection; Porphyromonas gingivalis; endothelial cell;
D O I
10.1016/j.atherosclerosis.2006.03.018
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:271 / 281
页数:11
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