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. 2018 Nov 27;9:2739. doi: 10.3389/fimmu.2018.02739

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Copyright © 2018 Maas, Soehnlein and Viola.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Neutrophil recruitment in the aorta. (1a) Neutrophil recruitment can be directed by platelets activated by oxidized LDL. The activated platelet adheres to the neutrophil, forming a platelet-neutrophil-aggregate. This aggregate formation is mediated by P-selectin. (1b) Neutrophils can also be activated by CCL5 released by activated platelets. (1c) Alternatively, upon damaged endothelium circulating neutrophils tether with ECs in a selectin-dependent manner, followed by their activation. (2) Activated neutrophils can release granular proteins, such as CRAMP and CatG, which can further support neutrophil recruitment. (3) CRAMP supports the recruitment via FPR (4) while CatG, seeded on the endothelium, facilitates firm adhesion of the neutrophil by engaging integrin clustering. (5) Platelets can also seed CCL5 on the endothelium, which can interact with CCR1 and CCR5 present on neutrophils, leading to the firm adhesion of neutrophils to the endothelium, and (6) eventually resulting in neutrophil extravasation. CatG, Cathepsin G; CCL, Chemokine (C-C motif) ligand; CCR, Chemokine (C-C motif) receptor; CRAMP, Cathelicidin related antimicrobial polypeptide; FPR, Formyl peptide receptor; ICAM-1, Intercellular adhesion molecule-1; oxLDL, Oxidized LDL.