title: Effects of Porphyromonas gingivalis antigens and proinflammatory cytokines on human coronary artery endothelial cells.
abstract: OBJECTIVE
  Individuals with periodontitis have been cited as having a significantly increased risk of developing coronary heart disease. Although accumulating evidence suggests that periodontal infection is involved in the development and progression of atherosclerosis, the underlying mechanisms remain to be elucidated. In the present study, we examined how periodontal infection could contribute to endothelial dysfunction.
  
  
  METHODS
  Human coronary arterial endothelial cells were stimulated with tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta, both of which are reported to be elevated in the serum of periodontitis patients. Cells were also stimulated with lipopolysaccharide, outer membrane protein and heat shock protein 60 derived from Porphyromonas gingivalis, a representative periodontopathic bacterium which is known to stimulate myeloid cells.
  
  
  RESULTS
  Although TNF-alpha and IL-1beta, at concentrations a little higher than those in sera of periodontitis patients, up-regulated the expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, P. gingivalis antigens had only a slight stimulatory effect.
  
  
  CONCLUSIONS
  Experiments in which the total pathogen burden is considered, rather than a single species of bacteria, would increase our understanding of the contribution of which periodontal infection to atherogenesis.
authors.affiliation: Periodontology and Immunology, Department of Oral Health and Welfare, Faculty of Dentistry, Niigata University, Niigata, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Honda
authors.forename: T
authors.initials: T
authors.lastname: Oda
authors.forename: H
authors.initials: H
authors.lastname: Yoshie
authors.forename: K
authors.initials: K
authors.lastname: Yamazaki
mesh_terms: D000942:Antigens, Bacterial / Q000502:physiology*; D001426:Bacterial Proteins / Q000502:physiology; D002478:Cells, Cultured; D003324:Coronary Artery Disease / Q000209:etiology; D003331:Coronary Vessels / Q000166:cytology / Q000378:metabolism*; D016207:Cytokines / Q000502:physiology; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism*; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology*; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D007375:Interleukin-1 / Q000502:physiology; D008070:Lipopolysaccharides / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000096:biosynthesis; D010518:Periodontitis / Q000150:complications; D016966:Porphyromonas gingivalis / Q000276:immunology* / Q000472:pathogenicity*; D011956:Receptors, Cell Surface / Q000096:biosynthesis; D051193:Toll-Like Receptors; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology; D015854:Up-Regulation; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D016207:Cytokines; D018836:Inflammation Mediators; D007375:Interleukin-1; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; D051193:Toll-Like Receptors; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1