Platelets: bridging hemostasis, inflammation, and immunity
TLDR
This review will highlight the central role platelets play in the initiation and modulation of the host inflammatory and immune responses.Abstract:
Although the function of platelets in the maintenance of hemostasis has been studied in great detail, more recent evidence has highlighted a central role for platelets in the host inflammatory and immune responses. Platelets by virtue of their large numbers and their ability to rapidly release a broad spectrum of immunomodulatory cytokines, chemokines, and other mediators act as circulating sentinels. Upon detection of a pathogen, platelets quickly activate and begin to drive the ensuing inflammatory response. Platelets have the ability to directly modulate the activity of neutrophils (phagocytosis, oxidative burst), endothelium (adhesion molecule and chemokine expression), and lymphocytes. Due to their diverse array of adhesion molecules and preformed chemokines, platelets are able to adhere to leukocytes and facilitate their recruitment to sites of tissue damage or infection. Furthermore, platelets directly participate in the capture and sequestration of pathogens within the vasculature. Platelet-neutrophil interactions are known to induce the release of neutrophil extracellular traps (NETs) in response to either bacterial or viral infection, and platelets have been shown to internalize pathogens, sequestering them in engulfment vacuoles. Finally, emerging data indicate that platelets also participate in the host immune response by directly killing infected cells. This review will highlight the central role platelets play in the initiation and modulation of the host inflammatory and immune responses.read more
Citations
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References
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Journal ArticleDOI
Neutrophil extracellular traps kill bacteria
Volker Brinkmann,Ulrike Reichard,Christian Goosmann,Beatrix Fauler,Yvonne Uhlemann,David S. Weiss,Yvette Weinrauch,Yvette Weinrauch,Arturo Zychlinsky +8 more
TL;DR: It is described that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria, which degrade virulence factors and kill bacteria.
Journal ArticleDOI
CD40 ligand on activated platelets triggers an inflammatory reaction of endothelial cells
Volker Henn,Joseph R. Slupsky,Michael Gräfe,Ioannis Anagnostopoulos,Reinhold Förster,Gert Müller-Berghaus,Richard A. Kroczek +6 more
TL;DR: In this paper, platelets express CD40L within seconds of activation in vitro and in the process of thrombus formation in vivo, indicating that platelets are not only involved in haemostasis but that they also directly initiate an inflammatory response of the vessel wall.
Journal ArticleDOI
Platelet TLR4 activates neutrophil extracellular traps to ensnare bacteria in septic blood
Stephen Clark,Adrienne C. Ma,Samantha A. Tavener,Braedon McDonald,Zahra Goodarzi,Margaret M. Kelly,Kamala D. Patel,Subhadeep Chakrabarti,Erin F. McAvoy,Gary D. Sinclair,Elizabeth Keys,Emma Allen-Vercoe,Rebekah DeVinney,Christopher J. Doig,Francis H. Y. Green,Paul Kubes +15 more
TL;DR: It is proposed that platelet TLR4 is a threshold switch for this new bacterial trapping mechanism in severe sepsis, where NETs have the greatest capacity for bacterial trapping.
Journal ArticleDOI
Platelets and the immune continuum
TL;DR: The mechanisms by which platelets contribute to immunity are discussed: these small cells are more immunologically savvy than the authors once thought.
Journal ArticleDOI
Platelets Amplify Inflammation in Arthritis via Collagen-Dependent Microparticle Production
Eric Boilard,Peter A. Nigrovic,Peter A. Nigrovic,Katherine Larabee,Gerald F. Watts,Jonathan S. Coblyn,Michael E. Weinblatt,Elena Massarotti,Eileen Remold-O'Donnell,Richard W. Farndale,Jerry Ware,David M. Lee +11 more
TL;DR: A previously unappreciated role for platelets and their activation-induced microparticles in inflammatory joint diseases is demonstrated and the collagen receptor glycoprotein VI is identified as a key trigger for platelet microparticle generation in arthritis pathophysiology.