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

DOI Web Site Web Site 12 Citations

Abstract

<jats:title>Summary</jats:title><jats:p>Evidence 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, <jats:italic>Porphyromonas gingivalis,</jats:italic> has the ability to aggregate human platelets in platelet‐rich plasma (PRP). Mechanism of <jats:italic>P. gingivalis</jats:italic>‐induced platelet aggregation in PRP was investigated. Proteinase inhibitors toward Arg‐gingipain (Rgp) and Lys‐gingipain (Kgp) did not suppress <jats:italic>P. gingivalis</jats:italic>‐induced platelet aggregation in PRP, whereas the Rgp inhibitor markedly inhibited <jats:italic>P. gingivalis</jats:italic>‐induced platelet aggregation using  washed  platelets.  Mutant  analysis  revealed  that <jats:italic>P. gingivalis</jats:italic>‐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 <jats:italic>P. gingivalis</jats:italic>‐induced platelet aggregation in PRP. <jats:italic>P. gingivalis</jats:italic> cell‐reactive IgG in plasma, and FcγRIIa receptor and to a lesser extent GPIbα receptor on platelets were found to be a prerequisite for <jats:italic>P. gingivalis</jats:italic>‐induced platelet aggregation in PRP. These results reveal a novel mechanism of platelet aggregation by <jats:italic>P. gingivalis</jats:italic>.</jats:p>

Journal

Citations (12)*help

See more

Related Projects

See more

Keywords

Details 詳細情報について

Report a problem

Back to top