Porphyromonas gingivalis‐induced platelet aggregation in plasma depends on Hgp44 adhesin but not Rgp proteinase

Abstract

SummaryEvidence from recent epidemiological studies suggests a link between periodontal infections and increased risk of atherosclerosis and related cardiovascular and cerebrovascular events in human subjects. One of the major pathogens of periodontitis, Porphyromonas gingivalis, has the ability to aggregate human platelets in platelet-rich plasma (PRP). Mechanism of P. gingivalis -induced platelet aggregation in PRP was investigated. Proteinase inhibitors toward Arg-gingipain (Rgp) and Lys-gingipain (Kgp) did not suppress P. gingivalis -induced platelet aggregation in PRP, whereas the Rgp inhibitor markedly inhibited P. gingivalis -induced platelet aggregation using washed platelets. Mutant analysis revealed that P. gingivalis -induced platelet aggregation in PRP depended on Rgp-, Kgp-and haemagglutinin A (HagA)-encoding genes that intragenically coded for adhesins such as Hgp44. Hgp44 adhesin on the bacterial cell surface, which was processed by Rgp and Kgp proteinases, was essential for P. gingivalisinduced platelet aggregation in PRP. P. gingivalis cellreactive IgG in plasma, and Fc γ γ γ γ RIIa receptor and to a lesser extent GPIb α α α α receptor on platelets were found to be a prerequisite for P. gingivalis -induced platelet aggregation in PRP. These results reveal a novel mechanism of platelet aggregation by P. gingivalis .

Platelet Interactions with Bacteria

“…Oral bacteria, Porphomonas gingivalis expresses a surface protein called hgp44 which induces platelet aggregation in an FcγRIIA dependent manner [73]. The authors demonstrated that IgG was critical for the interaction.…”

Platelet aggregation promoted by biofilms of oral bacteria and the effect of mouth rinses in vitro

“…Proteinase inhibitors of Arg-gingipain (Rgp) and Lys-gingipain (Kgp) did not suppress P. gingivalis-induced platelet aggregation in PRP, whereas the Rgp inhibitor markedly inhibited P. gingivalis-induced platelet aggregation when washed platelets were used. Mutant analysis revealed that P. gingivalis-induced platelet aggregation in PRP depended on Rgp-, Kgp-and hemagglutinin A (HagA)-encoding genes that intragenically coded for adhesins such as Hgp44 [25]. Future studies in our laboratory will focus on the molecular mechanisms of the signal pathway in P. gingivalis-induced platelet aggregation, since they are poorly understood.…”

Predisposition to Carotid Atherosclerosis in ICARAS Dental Substudy

“…5 Evidence from recent epidemiological studies suggests a link between periodontal infections and risk of vascular events. 6 DNA of typical periodontal pathogens was demonstrated in atheromatous plaques, and a low or moderate association between existing periodontitis and the development of vascular events had been observed. [5][6][7] Another crucial point deals with the socioeconomic status of the enrolled population being known that there is a relation between adverse socioeconomic conditions and both dental diseases and atherosclerosis.…”