Platelet TLR4 activates neutrophil extracellular traps to ensnare bacteria in septic blood

@article{Clark2007PlateletTA,
  title={Platelet TLR4 activates neutrophil extracellular traps to ensnare bacteria in septic blood},
  author={Stephen R. Clark and Adrienne C. Ma and Samantha A. Tavener and Braedon McDonald and Zahra S Goodarzi and Margaret M. Kelly and Kamala D Patel and Subhadeep Chakrabarti and Erin F. McAvoy and Gary D. Sinclair and Elizabeth Keys and Emma Allen-Vercoe and Rebekah Devinney and Christopher James Doig and Francis H Y Green and Paul Kubes},
  journal={Nature Medicine},
  year={2007},
  volume={13},
  pages={463-469}
}
It has been known for many years that neutrophils and platelets participate in the pathogenesis of severe sepsis, but the inter-relationship between these players is completely unknown. We report several cellular events that led to enhanced trapping of bacteria in blood vessels: platelet TLR4 detected TLR4 ligands in blood and induced platelet binding to adherent neutrophils. This led to robust neutrophil activation and formation of neutrophil extracellular traps (NETs). Plasma from severely… Expand
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References

SHOWING 1-10 OF 44 REFERENCES
Role of blood platelets in infection and inflammation.
  • M. Klinger, W. Jelkmann
  • Biology, Medicine
  • Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • 2002
Blood platelets are here presented as active players in antimicrobial host defense and the induction of inflammation and tissue repair in addition to their participation in hemostasis.Expand
Functional α4-integrin: A newly identified pathway of neutrophil recruitment in critically ill septic patients
TLDR
This pathway may provide a new therapeutic target to reduce inappropriate neutrophil adhesion without altering the normal yet critical β2-integrin–mediated adhesive function of neutrophils. Expand
Platelets express functional Toll-like receptor-4.
TLDR
It is demonstrated that although platelets do not increase P-selectin expression in response to LPS, platelets bind more avidly to fibrinogen under flow conditions in a Toll-like receptor-4 (TLR4)-dependent manner, which contribute to thrombocytopenia through neutrophil-dependent pulmonary sequestration in responseto LPS. Expand
Neutrophil Extracellular Traps Kill Bacteria
TLDR
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. Expand
Platelet function in sepsis
TLDR
The results suggest that sepsis alters the hemostatic function of the platelets and increases VEGF release in a thrombin‐independent manner. Expand
Neutrophil granule contents in the pathogenesis of lung injury
TLDR
The primary function of neutrophils in the innate immune response – to contain and kill invading microbial pathogens – is achieved through a series of rapid and coordinated responses culminating in phagocytosis and intracellular killing of the pathogens. Expand
Platelet‐induced neutrophil activation: platelet‐expressed fibrinogen induces the oxidative burst in neutrophils by an interaction with CD11C/CD18
TLDR
Fibrinogen and actin polymerization seem not to be required for the adhesion of neutrophils to platelets, whereas control peptides such as Gly‐His‐Arg‐Pro (GHRP) or Gly‐Pro‐Gly‐gly (GPGG) had no effect. Expand
An Endonuclease Allows Streptococcus pneumoniae to Escape from Neutrophil Extracellular Traps
TLDR
Pneumococci are trapped but, unlike many other pathogens, not killed by NETs, and it is demonstrated that escaping NETs promotes spreading of pneumococci from the upper airways to the lungs and from the lungs into the bloodstream during pneumonia. Expand
DNase Expression Allows the Pathogen Group A Streptococcus to Escape Killing in Neutrophil Extracellular Traps
TLDR
A significant role for NETs in neutrophil-mediated innate immunity is demonstrated, and a novel therapeutic target against invasive GAS infection is identified. Expand
Platelet Toll-like receptor expression modulates lipopolysaccharide-induced thrombocytopenia and tumor necrosis factor-alpha production in vivo.
TLDR
The results suggest that platelets express various TLRs and that the functional significance of one of these, TLR4, appears to be a role in the modulation of LPS-induced thrombocytopenia and TNF-alpha production, and implicates platelets as important mediators of innate immune responses against invading microorganisms. Expand
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4
5
...