Premium
Infection with a periodontal pathogen induces procoagulant effects in human aortic endothelial cells
Author(s) -
ROTH G. A.,
MOSER B.,
HUANG S. J.,
BRANDT J. S.,
HUANG Y.,
PAPAPANOU P. N.,
SCHMIDT A. M.,
LALLA E.
Publication year - 2006
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/j.1538-7836.2006.02128.x
Subject(s) - periodontal pathogen , porphyromonas gingivalis , pathogen , tissue factor , microbiology and biotechnology , plasminogen activator inhibitor 1 , biology , immunology , endothelial stem cell , tissue factor pathway inhibitor , plasminogen activator , periodontitis , coagulation , in vitro , medicine , endocrinology , biochemistry
Summary. 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.