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

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

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.

Detaljer

Författare
Enheter & grupper
Forskningsområden

Ämnesklassifikation (UKÄ) – OBLIGATORISK

  • Infektionsmedicin
Originalspråkengelska
Sidor (från-till)3515-3525
TidskriftInfection and Immunity
Volym83
Utgåva nummer9
StatusPublished - 2015
PublikationskategoriForskning
Peer review utfördJa

Relaterad forskningsoutput

Sinead Hurley, 2016, Division of Infection Medicine. 76 s.

Forskningsoutput: AvhandlingDoktorsavhandling (sammanläggning)

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