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Pneumolysin Mediates Platelet Activation In Vitro.

Jan Gert Nel1, Chrisna Durandt2, Timothy J Mitchell3

  • 1Department of Haematology, Faculty of Health Sciences, University of Pretoria and Tshwane Academic Division of the National Health Laboratory Service, PO Box 2034, Pretoria, 0001, South Africa. jan.nel@up.ac.za.

Lung
|May 20, 2016
PubMed
Summary
This summary is machine-generated.

Pneumolysin (Ply), a toxin from Streptococcus pneumoniae, activates human platelets by forming pores and increasing calcium influx. This platelet activation, marked by CD62P expression, may contribute to injury during pneumococcal disease.

Keywords:
CD62PCalciumCommunity-acquired pneumoniaP-selectinPneumococcusStreptococcus pneumoniae

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Area of Science:

  • * Microbiology
  • * Hematology
  • * Toxicology

Background:

  • * Invasive pneumococcal disease is a significant global health concern.
  • * Pneumolysin (Ply) is a key virulence factor produced by Streptococcus pneumoniae.
  • * The role of Ply in host-pathogen interactions, particularly platelet activation, remains incompletely understood.

Purpose of the Study:

  • * To investigate the direct effect of pneumolysin (Ply) on human platelet activation.
  • * To elucidate the mechanism by which Ply induces platelet activation.
  • * To assess the potential contribution of Ply-mediated platelet activation to disease pathogenesis.

Main Methods:

  • * Human platelets were exposed to varying concentrations of purified Ply.
  • * Platelet activation was assessed by measuring CD62P (P-selectin) expression via flow cytometry.
  • * Cytosolic calcium ion (Ca2+) concentrations were measured spectrofluorimetrically.
  • * Experiments were conducted with extracellular Ca2+ depletion and using a non-pore-forming pneumolysoid mutant.

Main Results:

  • * Ply significantly upregulated CD62P expression on platelets at concentrations of 40 ng/ml and higher.
  • * Ply exposure led to a marked increase in cytosolic Ca2+ concentrations, indicating Ca2+ influx.
  • * The pro-thrombotic effects of Ply on platelets were reduced by depleting extracellular Ca2+ or using a pore-deficient pneumolysoid.
  • * These findings suggest Ply activates platelets via sub-lytic pore formation and subsequent Ca2+ influx.

Conclusions:

  • * Pneumolysin directly activates human platelets through a mechanism involving pore formation and calcium influx.
  • * Mobilization of CD62P-expressing alpha-granules is a key event in Ply-induced platelet activation.
  • * Ply-mediated platelet activation may play a role in the pathogenesis of acute lung and myocardial injury associated with invasive pneumococcal disease.