Interactions of Porphyromonas gingivalis with Host Cells: Implications for Cardiovascular Diseases

Background: Recent epidemiological studies have suggested a contribution of periodontitis in atherosclerotic diseases. Two mechanisms have been proposed to explain such a connection involving general inflammatory responses and/or specific effects of periodontal bacteria on host tissues. Methods: The...

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Bibliographic Details
Published in:Journal of periodontology (1970) 2003-01, Vol.74 (1), p.85-89
Main Authors: Kuramitsu, Howard K., Kang, In‐Chol, Qi, Minshan
Format: Article
Language:English
Subjects:
Animals
Arteriosclerosis - microbiology
Atherosclerotic diseases/etiology
Cell Culture Techniques
Cell Line
Chemokine CCL2 - physiology
Dentistry
Endothelium, Vascular - cytology
Endothelium, Vascular - microbiology
Escherichia coli
fimbriae
Fimbriae Proteins - physiology
Fimbriae, Bacterial - physiology
Foam Cells - microbiology
Humans
Lipopolysaccharides - pharmacology
Lipoproteins, LDL - physiology
Macrophages - microbiology
Mice
Periodontitis - microbiology
Pili, Sex - physiology
Porphyromonas gingivalis
Porphyromonas gingivalis - physiology
Salmonella typhimurium
Umbilical Veins - cytology
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Summary:Background: Recent epidemiological studies have suggested a contribution of periodontitis in atherosclerotic diseases. Two mechanisms have been proposed to explain such a connection involving general inflammatory responses and/or specific effects of periodontal bacteria on host tissues. Methods: The role of the periodontopathogen Porphyromonas gingivalis as a potential contributor to atherosclerosis has been investigated in model systems using human umbilical vein endothelial cells (HUVEC) and murine J774 macrophage cell cultures. Results: P. gingivalis 381 was demonstrated to induce foam cell formation in J774 macrophage cell cultures in the presence of low‐density lipoproteins. The active bacterial component involved in this process appears to be lipopolysaccharide. This effect was not limited to these organisms as several other Gram‐positive and Gram‐negative oral bacteria exhibited the same property. In addition, in a more specific manner, P. gingivalis induced monocyte chemoattractant protein‐1 secretion in HUVEC cultures. Conclusions: The fimbriae of strain 381 are important, but are not required, for this inductive effect. Taken together, these results suggest a potential role for P. gingivalis in several steps involved in atherosclerotic lesion formation. J Periodontol 2003; 74:85‐89.
ISSN:0022-3492
1943-3670
DOI:10.1902/jop.2003.74.1.85