Platelets protect from septic shock by inhibiting macrophage-dependent inflammation via the cyclooxygenase 1 signalling pathway

Nat Commun. 2013:4:2657. doi: 10.1038/ncomms3657.

Abstract

Although it has long been known that patients with sepsis often have thrombocytopenia and that septic patients with severe thrombocytopenia have a poor prognosis and higher mortality, the role of platelets in the pathogenesis of sepsis is poorly understood. Here we report a protective role of platelets in septic shock. We show that experimental thrombocytopenia induced by intraperitoneal injection of an anti-glycoprotein Ibα monoclonal antibody increases mortality and aggravates organ failure, whereas transfusion of platelets reduces mortality in lipopolysaccharide-induced endotoxemia and a bacterial infusion mouse sepsis model. Plasma concentrations of proinflammatory cytokines TNF-α and IL-6 are elevated by thrombocytopenia and decreased by platelet transfusion in septic mice. Furthermore, we identify that platelets protect from septic shock by inhibiting macrophage-dependent inflammation via the COX1/PGE₂/EP4-dependent pathway. Thus, these findings demonstrate a previously unappreciated role for platelets in septic shock and suggest that platelet transfusion may be effective in treating severely septic patients.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Antibodies, Anti-Idiotypic / pharmacology
  • Blood Platelets / cytology
  • Blood Platelets / immunology*
  • Cyclooxygenase 1 / genetics
  • Cyclooxygenase 1 / immunology
  • Dinoprostone / genetics
  • Dinoprostone / immunology
  • Disease Models, Animal
  • Gene Expression Regulation
  • Humans
  • Inflammation / chemically induced
  • Inflammation / genetics
  • Inflammation / pathology
  • Inflammation / prevention & control
  • Interleukin-6 / biosynthesis
  • Interleukin-6 / immunology
  • Lipopolysaccharides / pharmacology
  • Macrophages, Peritoneal / drug effects
  • Macrophages, Peritoneal / immunology*
  • Macrophages, Peritoneal / pathology
  • Male
  • Membrane Proteins / genetics
  • Membrane Proteins / immunology
  • Mice
  • Mice, Inbred C57BL
  • Platelet Glycoprotein GPIb-IX Complex / immunology
  • Platelet Transfusion*
  • Receptors, Prostaglandin E, EP4 Subtype / genetics
  • Receptors, Prostaglandin E, EP4 Subtype / immunology
  • Shock, Septic / chemically induced
  • Shock, Septic / genetics
  • Shock, Septic / pathology
  • Shock, Septic / therapy*
  • Signal Transduction
  • Thrombocytopenia / chemically induced
  • Thrombocytopenia / genetics
  • Thrombocytopenia / pathology
  • Thrombocytopenia / prevention & control*
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / immunology

Substances

  • Antibodies, Anti-Idiotypic
  • Interleukin-6
  • Lipopolysaccharides
  • Membrane Proteins
  • Platelet Glycoprotein GPIb-IX Complex
  • Ptger4 protein, mouse
  • Receptors, Prostaglandin E, EP4 Subtype
  • Tumor Necrosis Factor-alpha
  • Cyclooxygenase 1
  • Ptgs1 protein, mouse
  • Dinoprostone