title: Infection with a periodontal pathogen induces procoagulant effects in human aortic endothelial cells.
abstract: BACKGROUND
  Multiple studies have demonstrated a link between periodontal infections and vascular disease. Porphyromonas gingivalis, a major periodontal pathogen, has been shown to adhere to and invade endothelial cells.
  
  
  OBJECTIVE
  In order to dissect mechanisms underlying these observations, we assessed the role of P. gingivalis infection in modulating properties of endothelial cells linked to atherothrombosis.
  
  
  METHODS
  Primary human aortic endothelial cells (HAEC) were infected with either P. gingivalis 381 or its non-invasive fimbriae-deficient mutant, DPG3. Markers of coagulation and thrombosis were assessed 8 h and 18 h postinfection in cell lysates and supernatants.
  
  
  RESULTS
  Infection with P. gingivalis 381 significantly enhanced tissue factor expression and activity, and suppressed levels of tissue factor pathway inhibitor. Furthermore, P. gingivalis infection decreased levels and activity of tissue plasminogen activator, and enhanced plasminogen activator inhibitor-1 antigen and activity. Consistent with an important role for bacterial adhesion/invasion in this setting, infection with DPG3 failed to induce procoagulant properties in HAEC. Most of the above effects of P. gingivalis 381 were more apparent at the later time point (18 h postinfection). This suggests that P. gingivalis infection, rather than having an immediate and direct effect, might activate pathways that, in turn, trigger endothelial procoagulant mechanisms.
  
  
  CONCLUSIONS
  Taken together these data demonstrate for the first time that infection with a periodontal pathogen induces procoagulant responses in HAEC.
authors.affiliation: Department of Surgery, Division of Surgical Science, College of Physicians and Surgeons, New York, NY 10032, USA.
authors.forename: G A
authors.initials: GA
authors.lastname: Roth
authors.forename: B
authors.initials: B
authors.lastname: Moser
authors.forename: S J
authors.initials: SJ
authors.lastname: Huang
authors.forename: J S
authors.initials: JS
authors.lastname: Brandt
authors.forename: Y
authors.initials: Y
authors.lastname: Huang
authors.forename: P N
authors.initials: PN
authors.lastname: Papapanou
authors.forename: A M
authors.initials: AM
authors.lastname: Schmidt
authors.forename: E
authors.initials: E
authors.lastname: Lalla
mesh_terms: D001011:Aorta / Q000382:microbiology*; D001422:Bacterial Adhesion; D016866:Bacteroidaceae Infections / Q000473:pathology*; D001777:Blood Coagulation; D002478:Cells, Cultured; D003029:Coagulants / Q000378:metabolism; D004730:Endothelium, Vascular / Q000382:microbiology*; D006801:Humans; D009154:Mutation; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D016966:Porphyromonas gingivalis / Q000378:metabolism*; D013925:Thromboplastin / Q000378:metabolism; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000096:biosynthesis / Q000378:metabolism
chemical_list: D003029:Coagulants; D017395:Plasminogen Activator Inhibitor 1; D013925:Thromboplastin; D010959:Tissue Plasminogen Activator