Invasion of human vascular endothelial cells by Actinobacillus actinomycetemcomitans via the receptor for platelet-activating factor.
Strains of the periodontal pathogen Actinobacillus actinomycetemcomitans are variable with respect to display of phosphorylcholine (PC)-bearing antigens. We have examined strains of A. actinomycetemcomitans with and without PC to assess their ability to invade endothelial cells via the receptor for platelet-activating factor (PAF). Results of antibiotic protection assays indicate that PC-bearing A. actinomycetemcomitans invade human vascular endothelial cells by a mechanism inhibitable by CV3988, a PAF receptor antagonist, and by PAF itself. The invasive phenotype was verified by transmission electron microscopy. A PC-deficient strain of this organism was not invasive. This property, in addition to the established ability of A. actinomycetemcomitans to invade epithelial cells, may provide this organism with access to the systemic circulation. The ability of PC-bearing oral bacteria to access the circulation may also explain the elevated levels of anti-PC antibody in serum found in patients with periodontitis.
Schenkein
H A
HA
Clinical Research Center for Periodontal Diseases, School of Dentistry, Virginia Commonwealth University, Richmond, Virginia 23298, USA. hschenke@hsc.vcu.edu
Barbour
S E
SE
Berry
C R
CR
Kipps
B
B
Tew
J G
JG
D016976:Aggregatibacter actinomycetemcomitans / Q000472:pathogenicity*; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology / Q000382:microbiology*; D006801:Humans; D010767:Phosphorylcholine / Q000276:immunology; D010980:Platelet Membrane Glycoproteins / Q000502:physiology*; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled
D010980:Platelet Membrane Glycoproteins; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; C039351:platelet activating factor receptor; D010767:Phosphorylcholine