Platelet–Neutrophil Crosstalk in Thrombosis

Abstract

Platelets are essential for the formation of a haemostatic plug to prevent bleeding, while neutrophils are the guardians of our immune defences against invading pathogens. The interplay between platelets and innate immunity, and subsequent triggering of the activation of coagulation is part of the host system to prevent systemic spread of pathogen in the blood stream. Aberrant immunothrombosis and excessive inflammation can however, contribute to the thrombotic burden observed in many cardiovascular diseases. In this review, we highlight how platelets and neutrophils interact with each other and how their crosstalk is central to both arterial and venous thrombosis and in COVID-19. While targeting platelets and coagulation enables efficient antithrombotic treatments, they are often accompanied with a bleeding risk. We also discuss how novel approaches to reduce platelet-mediated recruitment of neutrophils could represent promising therapies to treat thrombosis without affecting haemostasis.

Neutrophil extracellular traps formation is associated with postoperative complications in neonates and infants undergoing congenital cardiac surgery

“…Neutrophils and platelets are two major cell types responsible for thrombosis formation 23,35-37 . Our statistical analysis did not reveal any significant differences between the two groups, neither in the overall cohort ( Suppl Fig.…”

“…Neutrophils and platelets are two major cell types responsible for thrombosis formation 23,[35][36][37] .…”

“…However, their robust effector functions can damage tissues 21 . For example, they can induce NETs and cause microthrombosis [22][23][24][25] . Elevated levels of DAMPs have been positively correlated with systemic inflammatory response syndrome (SIRS) and multiple organ injury in trauma and sepsis patients 19,26 .…”

Immune gene polymorphisms associated with poor response to platelet transfusion and recombinant factor VII administration in Glanzmann thrombasthenia

“…37 Platelets can also adhere to leukocytes via αIIbβ3 under inflammatory conditions. 38 Consequently, platelets contribute to immune functions by premRNA splicing of some mediators like interleukin-1β, activating immune cells. 36 We found a higher incidence of rs3783553, rs3783550, rs3917356 and rs2234663 polymorphisms in interleukin-1 gene in GT patients which suggest a possible link between GT progression and interleukin-1 gene polymorphisms, requiring further investigation.…”

“…Activated platelets release interleukin‐1β, a cytokine that initiates immune response 37 . Platelets can also adhere to leukocytes via αIIbβ3 under inflammatory conditions 38 . Consequently, platelets contribute to immune functions by premRNA splicing of some mediators like interleukin‐1β, activating immune cells 36 .…”