Neutrophils scan for activated platelets to initiate inflammation

Vinatha Sreeramkumar; José M. Adrover; Ivan Ballesteros; Maria Isabel Cuartero; Jan Rossaint; Izaskun Bilbao; Maria Nácher; Christophe Pitaval; Irena Radovanovic; Yoshinori Fukui; Rodger P. McEver; Marie Dominique Filippi; Ignacio Lizasoain; Jesús Ruiz-Cabello; Alexander Zarbock; María A. Moro; Andrés Hidalgo

doi:10.1126/science.1256478

Neutrophils scan for activated platelets to initiate inflammation

Vinatha Sreeramkumar, José M. Adrover, Ivan Ballesteros, Maria Isabel Cuartero, Jan Rossaint, Izaskun Bilbao, Maria Nácher, Christophe Pitaval, Irena Radovanovic, Yoshinori Fukui, Rodger P. McEver, Marie Dominique Filippi, Ignacio Lizasoain, Jesús Ruiz-Cabello, Alexander Zarbock, María A. Moro, Andrés Hidalgo

Department of Immunobiology and Neuroscience

Research output: Contribution to journal › Article › peer-review

470 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	1234-1238
Number of pages	5
Journal	Science
Volume	346
Issue number	6214
DOIs	https://doi.org/10.1126/science.1256478
Publication status	Published - Dec 5 2014

All Science Journal Classification (ASJC) codes

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Sreeramkumar, V., Adrover, J. M., Ballesteros, I., Cuartero, M. I., Rossaint, J., Bilbao, I., Nácher, M., Pitaval, C., Radovanovic, I., Fukui, Y., McEver, R. P., Filippi, M. D., Lizasoain, I., Ruiz-Cabello, J., Zarbock, A., Moro, M. A., & Hidalgo, A. (2014). Neutrophils scan for activated platelets to initiate inflammation. Science, 346(6214), 1234-1238. https://doi.org/10.1126/science.1256478

Sreeramkumar, V, Adrover, JM, Ballesteros, I, Cuartero, MI, Rossaint, J, Bilbao, I, Nácher, M, Pitaval, C, Radovanovic, I, Fukui, Y, McEver, RP, Filippi, MD, Lizasoain, I, Ruiz-Cabello, J, Zarbock, A, Moro, MA & Hidalgo, A 2014, 'Neutrophils scan for activated platelets to initiate inflammation', Science, vol. 346, no. 6214, pp. 1234-1238. https://doi.org/10.1126/science.1256478

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title = "Neutrophils scan for activated platelets to initiate inflammation",

abstract = "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.",

author = "Vinatha Sreeramkumar and Adrover, {Jos{\'e} M.} and Ivan Ballesteros and Cuartero, {Maria Isabel} and Jan Rossaint and Izaskun Bilbao and Maria N{\'a}cher and Christophe Pitaval and Irena Radovanovic and Yoshinori Fukui and McEver, {Rodger P.} and Filippi, {Marie Dominique} and Ignacio Lizasoain and Jes{\'u}s Ruiz-Cabello and Alexander Zarbock and Moro, {Mar{\'i}a A.} and Andr{\'e}s Hidalgo",

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AU - Sreeramkumar, Vinatha

AU - Adrover, José M.

AU - Ballesteros, Ivan

AU - Cuartero, Maria Isabel

AU - Rossaint, Jan

AU - Bilbao, Izaskun

AU - Nácher, Maria

AU - Pitaval, Christophe

AU - Radovanovic, Irena

AU - Fukui, Yoshinori

AU - McEver, Rodger P.

AU - Filippi, Marie Dominique

AU - Lizasoain, Ignacio

AU - Ruiz-Cabello, Jesús

AU - Zarbock, Alexander

AU - Moro, María A.

AU - Hidalgo, Andrés

PY - 2014/12/5

Y1 - 2014/12/5

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AB - 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.

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Neutrophils scan for activated platelets to initiate inflammation

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