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Single platelets seal neutrophil-induced vascular breaches via GPVI during immune-complex-mediated inflammation in mice.
Gros, Angèle; Syvannarath, Varouna; Lamrani, Lamia; Ollivier, Véronique; Loyau, Stéphane; Goerge, Tobias; Nieswandt, Bernhard; Jandrot-Perrus, Martine; Ho-Tin-Noé, Benoît.
Afiliação
  • Gros A; INSERM Unit 1148, University Paris Diderot, Paris, France; Laboratory for Vascular Translational Science, Sorbonne Paris Cité, Paris, France;
  • Syvannarath V; INSERM Unit 1148, University Paris Diderot, Paris, France; Laboratory for Vascular Translational Science, Sorbonne Paris Cité, Paris, France;
  • Lamrani L; INSERM Unit 1148, University Paris Diderot, Paris, France; Laboratory for Vascular Translational Science, Sorbonne Paris Cité, Paris, France;
  • Ollivier V; INSERM Unit 1148, University Paris Diderot, Paris, France; Laboratory for Vascular Translational Science, Sorbonne Paris Cité, Paris, France;
  • Loyau S; INSERM Unit 1148, University Paris Diderot, Paris, France; Laboratory for Vascular Translational Science, Sorbonne Paris Cité, Paris, France;
  • Goerge T; Department of Dermatology, University Hospital of Münster, Münster, Germany; Interdisciplinary Center for Clinical Research (IZKF), University of Münster, Münster, Germany; and.
  • Nieswandt B; Department of Vascular Medicine, University Hospital and Rudolf Virchow Center, Würzburg, Germany.
  • Jandrot-Perrus M; INSERM Unit 1148, University Paris Diderot, Paris, France; Laboratory for Vascular Translational Science, Sorbonne Paris Cité, Paris, France;
  • Ho-Tin-Noé B; INSERM Unit 1148, University Paris Diderot, Paris, France; Laboratory for Vascular Translational Science, Sorbonne Paris Cité, Paris, France;
Blood ; 126(8): 1017-26, 2015 Aug 20.
Article em En | MEDLINE | ID: mdl-26036804
Platelets protect vascular integrity during inflammation. Recent evidence suggests that this action is independent of thrombus formation and requires the engagement of glycoprotein VI (GPVI), but it remains unclear how platelets prevent inflammatory bleeding. We investigated whether platelets and GPVI act primarily by preventing detrimental effects of neutrophils using models of immune complex (IC)-mediated inflammation in mice immunodepleted in platelets and/or neutrophils or deficient in GPVI. Depletion of neutrophils prevented bleeding in thrombocytopenic and GPVI(-/-) mice during IC-mediated dermatitis. GPVI deficiency did not modify neutrophil recruitment, which was reduced by thrombocytopenia. Neutrophil cytotoxic activities were reduced in thrombocytopenic and GPVI(-/-) mice during IC-mediated inflammation. Intravital microscopy revealed that in this setting, intravascular binding sites for platelets were exposed by neutrophils, and GPVI supported the recruitment of individual platelets to these spots. Furthermore, the platelet secretory response accompanying IC-mediated inflammation was partly mediated by GPVI, and blocking of GPVI signaling impaired the vasculoprotective action of platelets. Together, our results show that GPVI plays a dual role in inflammation by enhancing neutrophil-damaging activities while supporting the activation and hemostatic adhesion of single platelets to neutrophil-induced vascular breaches.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Plaquetas / Glicoproteínas da Membrana de Plaquetas / Doenças do Complexo Imune / Inflamação / Neutrófilos Limite: Animals Idioma: En Revista: Blood Ano de publicação: 2015 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Plaquetas / Glicoproteínas da Membrana de Plaquetas / Doenças do Complexo Imune / Inflamação / Neutrófilos Limite: Animals Idioma: En Revista: Blood Ano de publicação: 2015 Tipo de documento: Article