2026-06-14T05:05:35Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/51762024-09-27T09:47:49Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Rossaint, Jan
author
Kuehne, Katharina
author
Skupski, Jennifer
author
Van Aken, Hugo
author
Looney, Mark R.
author
Hidalgo, Andres
author
Zarbock, Alexander
funder
Deutsche Forschungsgemeinschaft (Alemania)
funder
University of Münster (Alemania)
funder
Ministerio de Economía y Competitividad (España)
funder
NIH - National Heart, Lung, and Blood Institute (NHLBI) (Estados Unidos)
funder
Fundación ProCNIC
2017-10-20T10:33:51Z
2017-10-20T10:33:51Z
2016
Nat Commun. 2016; 7:13464
10.1038/ncomms13464
2041-1723
Nature Communicacions
27845343
http://hdl.handle.net/20.500.12105/5176
The innate immune response to bacterial infections requires the interaction of neutrophils and platelets. Here, we show that a multistep reciprocal crosstalk exists between these two cell types, ultimately facilitating neutrophil influx into the lung to eliminate infections. Activated platelets adhere to intravascular neutrophils through P-selectin/P-selectin glycoprotein ligand-1 (PSGL-1)-mediated binding, a primary interaction that allows platelets glycoprotein Ib alpha (GPIb alpha)-induced generation of neutrophil-derived extracellular vesicles (EV). EV production is directed by exocytosis and allows shuttling of arachidonic acid into platelets. EVs are then specifically internalized into platelets in a Mac1-dependent fashion, and relocated into intracellular compartments enriched in cyclooxygenase1 (Cox1), an enzyme processing arachidonic acid to synthesize thromboxane A(2) (TxA(2)). Finally, platelet-derived-TxA(2) elicits a full neutrophil response by inducing the endothelial expression of ICAM-1, intravascular crawling, and extravasation. We conclude that critical substrate-enzyme pairs are compartmentalized in neutrophils and platelets during steady state limiting non-specific inflammation, but bacterial infection triggers regulated EV shuttling resulting in robust inflammation and pathogen clearance.
eng
ACUTE LUNG INJURY
GLYCOPROTEIN IB-ALPHA
RESPIRATORY-DISTRESS-SYNDROME
P-SELECTIN
POLYMORPHONUCLEAR LEUKOCYTES
PROSTAGLANDIN E-2
INTEGRIN MAC-1
UP-REGULATION
KAPPA-B
INFLAMMATION
Directed transport of neutrophil-derived extracellular vesicles enables platelet-mediated innate immune response
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