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Platelet-streptococcal interactions in endocarditis

M C Herzberg1

  • 1Department of Preventive Sciences, School of Dentistry, University of Minnesota, Minneopolis 55455, USA.

Critical Reviews in Oral Biology and Medicine : an Official Publication of the American Association of Oral Biologists
|January 1, 1996
PubMed
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It is time to move on.....

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The platelet aggregation-associated protein (PAAP) of Streptococcus sanguis directly contributes to infective endocarditis by promoting platelet accumulation and bacterial colonization on heart valves. Neutralizing PAAP reduces disease severity, highlighting its critical role in pathogenesis.

Area of Science:

  • Microbiology
  • Cardiovascular Medicine
  • Pathogen-Host Interactions

Background:

  • Infective endocarditis involves bacterial formation of septic masses on heart valves, commonly caused by viridans streptococci.
  • Bacterial factors like adhesins and exopolysaccharides contribute to streptococcal infectivity and pathogenicity in endocarditis.

Purpose of the Study:

  • To elucidate the role of the platelet aggregation-associated protein (PAAP) from Streptococcus sanguis in the pathogenesis of experimental infective endocarditis.
  • To understand the mechanism by which PAAP contributes to bacterial colonization and vegetation formation on heart valves.

Main Methods:

  • Investigated the function of PAAP, a rhamnose-rich glycoprotein expressed on the cell wall of aggregation-inducing S. sanguis strains.
  • Examined PAAP interaction with platelet receptors, including alpha 2-integrin-associated protein and collagen-binding components.

Related Experiment Videos

  • Proposed a mechanistic model for PAAP's role in platelet accumulation and bacterial colonization on injured heart valves.

    • Main Results:

    • PAAP enhances platelet accumulation on injured heart valves, facilitating Streptococcus sanguis colonization within fibrin-enmeshed thrombi (vegetations).
    • PAAP expression is modulated by heat shock and collagen, suggesting adaptive responses during infection.
    • Experimental endocarditis severity and vegetation size are reduced when PAAP is unexpressed or neutralized by antibodies.

    Conclusions:

    • PAAP is a key virulence factor in Streptococcus sanguis-induced infective endocarditis, directly contributing to vegetation development and valvular pathology.
    • PAAP's function may overlap with other adhesins, playing a crucial role in both bacterial colonization and thrombus formation.
    • Targeting PAAP presents a potential therapeutic strategy for mitigating infective endocarditis severity.