Platelet-dependent neutrophil function is dysregulated by M protein from Streptococcus pyogenes.

Sinead Hurley, Fredrik Kahn, Pontus Nordenfelt, Matthias Mörgelin, Ole E Sørensen, Oonagh Shannon

Research output: Contribution to journalArticlepeer-review

Abstract

Platelets are rapidly responsive sentinel cells that patrol the bloodstream and contribute to the host response to infection. Platelets have been reported to form heterotypic aggregates with leukocytes and may modulate their function. Herein we have investigated platelet-neutrophil complex formation and neutrophil function in response to distinct agonists. The endogenous platelet activator thrombin gave rise to platelet-dependent neutrophil activation, resulting in enhanced phagocytosis and bacterial killing. Streptococcus pyogenes is an important causative agent of severe infectious disease, which can manifest as sepsis and septic shock. M1 protein from S. pyogenes also mediated platelet-neutrophil complex formation, however these neutrophils were dysfunctional and exhibited diminished chemotactic ability and bacterial killing. This reveals an important agonist dependent neutrophil dysfunction during platelet-neutrophil complex formation, and highlights the role of platelets during the immune response to streptococcal infection.
Original languageEnglish
Pages (from-to)3515-3525
JournalInfection and Immunity
Volume83
Issue number9
DOIs
Publication statusPublished - 2015

Subject classification (UKÄ)

  • Infectious Medicine

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