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 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.
Kuramitsu
Howard K
HK
Department of Oral Biology, University at Buffalo, Buffalo, NY 14214, USA.
Kang
In-Chol
IC
Qi
Minshan
M
D000818:Animals; D001161:Arteriosclerosis / Q000382:microbiology*; D018929:Cell Culture Techniques; D002460:Cell Line; D018932:Chemokine CCL2 / Q000502:physiology; D004730:Endothelium, Vascular / Q000166:cytology / Q000382:microbiology; D004926:Escherichia coli; D036781:Fimbriae Proteins / Q000502:physiology; D010861:Fimbriae, Bacterial / Q000502:physiology; D005487:Foam Cells / Q000382:microbiology; D006801:Humans; D008070:Lipopolysaccharides / Q000494:pharmacology; D008077:Lipoproteins, LDL / Q000502:physiology; D008264:Macrophages / Q000382:microbiology; D051379:Mice; D010518:Periodontitis / Q000382:microbiology*; D018933:Pili, Sex / Q000502:physiology; D016966:Porphyromonas gingivalis / Q000502:physiology*; D012486:Salmonella typhimurium; D014471:Umbilical Veins / Q000166:cytology
D018932:Chemokine CCL2; D008070:Lipopolysaccharides; D008077:Lipoproteins, LDL; C063055:fimbrillin; D036781:Fimbriae Proteins