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Pneumolysin mediates heterotypic aggregation of neutrophils and platelets in vitro. | LitMetric

Pneumolysin mediates heterotypic aggregation of neutrophils and platelets in vitro.

J Infect

Department of Immunology, Faculty of Health Sciences, University of Pretoria, Pretoria, South Africa; Institute for Cellular and Molecular Medicine, South African Medical Research Council Unit for Stem Cell Research, Department of Immunology, Faculty of Health Sciences, University of Pretoria, Pretoria, South Africa.

Published: June 2017

AI Article Synopsis

  • This study investigates how the pneumococcal toxin pneumolysin (Ply) affects neutrophils and their interactions with platelets, which may worsen damage in severe infections.
  • Researchers found that Ply increases the production of platelet-activating factor (PAF) and thromboxane A (TxA) in neutrophils, with significant effects seen at specific toxin concentrations.
  • Although Ply enhances aggregation of neutrophils and platelets, this process does not involve PAF or TxA, but relies on other factors like P-selectin and PAR1, indicating a complex mechanism of inflammation.

Article Abstract

Objectives: Platelets orchestrate the inflammatory activities of neutrophils, possibly contributing to pulmonary and myocardial damage during severe pneumococcal infection. This study tested the hypothesis that the pneumococcal toxin, pneumolysin (Ply), activates production of platelet-activating factor (PAF) and thromboxane A (TxA) by neutrophils, these bioactive lipids being potential mediators of neutrophil:platelet (NP) networking.

Methods: The effects of recombinant Ply (10-80 ng mL) on the production of PAF and TxA by isolated neutrophils were measured using ELISA procedures, and NP aggregation by flow cytometry.

Results: Exposure of neutrophils to Ply induced production of PAF and, to a lesser extent, TxA, achieving statistical significance at ≥20 ng mL of the toxin. In the case of NP interactions, Ply promoted heterotypic aggregation which was dependent on upregulation of P-selectin (CD62P) and activation of protease-activated receptor 1 (PAR1), attaining statistical significance at ≥10 ng mL of the toxin, but did not involve either PAF or TxA.

Conclusion: Ply induces synthesis of PAF and TxA by human neutrophils, neither of which appears to contribute to the formation of NP heterotypic aggregates in vitro, a process which is seemingly dependent on CD62P and PAR1. These pro-inflammatory activities of Ply may contribute to the pathogenesis of pulmonary and myocardial injury during severe pneumococcal infection.

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Source
http://dx.doi.org/10.1016/j.jinf.2017.02.010DOI Listing

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