sábado, 6 de diciembre de 2014

Neutrophils scan for activated platelets to initiate inflammation

Neutrophils scan for activated platelets to initiate inflammation



Science
Vol. 346 no. 6214 pp. 1234-1238 
DOI: 10.1126/science.1256478
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Neutrophils scan for activated platelets to initiate inflammation

  1. Andrés Hidalgo1,9,*
+Author Affiliations
  1. 1Department of Atherothrombosis, Imaging and Epidemiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
  2. 2Unidad de Investigación Neurovascular, Department of Pharmacology, Faculty of Medicine, Universidad Complutense and Instituto de Investigación Hospital 12 de Octubre (i+12), Madrid, Spain.
  3. 3Department of Anesthesiology and Critical Care Medicine, University of Münster and Max Planck Institute Münster, Münster, Germany.
  4. 4Ciber de Enfermedades Respiratorias (CIBERES), Madrid, Spain.
  5. 5Faculty of Science, Medicine and Health, University of Wollongong, New South Wales, Australia.
  6. 6Division of Immunogenetics, Department of Immunobiology and Neuroscience, Kyushu University, Japan.
  7. 7Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.
  8. 8Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Research Foundation, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
  9. 9Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany.
  1. *Corresponding author. E-mail: ahidalgo@cnic.es
Immune and inflammatory responses require leukocytes to migrate within and through the vasculature, a process that is facilitated by their capacity to switch to a polarized morphology with an asymmetric distribution of receptors. We report that neutrophil polarization within activated venules served to organize a protruding domain that engaged activated platelets present in the bloodstream. The selectin ligand PSGL-1 transduced signals emanating from these interactions, resulting in the redistribution of receptors that drive neutrophil migration. Consequently, neutrophils unable to polarize or to transduce signals through PSGL-1 displayed aberrant crawling, and blockade of this domain protected mice against thromboinflammatory injury. These results reveal that recruited neutrophils scan for activated platelets, and they suggest that the neutrophils’ bipolarity allows the integration of signals present at both the endothelium and the circulation before inflammation proceeds.
  • Received for publication 27 May 2014.
  • Accepted for publication 7 November 2014.


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