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 Blood, 21 May 2009, Vol. 113, No. 21, pp. 5254-5265.
Prepublished online as a Blood First Edition Paper on March 4, 2009; DOI 10.1182/blood-2008-09-180794.

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Submitted September 25, 2008
Accepted February 10, 2009

Neutrophils phagocytose activated platelets in vivo: a phosphatidylserine, P-selectin and {beta}2 integrin-dependent cell clearance program

Norma Maugeri*, Patrizia Rovere-Querini, Virgilio Evangelista, Cesare Covino, Annalisa Capobianco, Maria T.S. Bertilaccio, Antonio Piccoli, Licia Totani, Domenico Cianflone, Attilio Maseri, and Angelo A. Manfredi

H San Raffaele Scientific Institute and University Vita-Salute San Raffaele, Milano, Italy
Laboratory of Vascular Biology and Pharmacology, Consorzio Mario Negri Sud, Santa Maria Imbaro, Italy

* Corresponding author; email: maugeri.norma{at}hsr.it.

Activated platelets express ligands, which are recognized by counter-receptors on neutrophils. Here, we show that the ensuing cell-to-cell interaction programs neutrophil phagocytic function, resulting in activated platelet clearance. Neutrophils that have internalised platelets circulate in the blood of patients with acute myocardial infarction, and the extent of platelet clearance correlates with expression of platelet activation, including P-selectin. Activated platelets injected e.v. in experimental animals are detectable into circulating neutrophils 60 minutes after, and within 3 hours >70 % circulating neutrophils have internalized platelets. Platelet clearance comprises two events: adhesion to neutrophils, which requires divalent cations and depends on P-selectin, on the P-selectin glycoprotein ligand-1 (PSGL-1), and on the CD11b/CD18 {beta}2-integrin; internalization, which is abrogated by the phosphatidylserine-binding protein Annexin A5. Adhesion to platelets causes neutrophil degranulation and is blocked by antibodies specific for P-selectin and PSGL-1, either in a synthetic medium in vitro or in the whole blood, therefore in the presence of a physiological array of plasma cofactors and opsonins. The data suggest that the interaction between circulating platelets and neutrophils influences innate immune functions, possibly contributing to regulate vascular inflammation.


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