title: Aspirin and P2Y12 Inhibitors in platelet-mediated activation of neutrophils and monocytes.
abstract: Platelets are key players in haemostasis and represent a pivotal link between inflammation, immunity and atherogenesis. Depending on the (patho)physiological environment platelets modulate various leukocyte functions via release of inflammatory mediators and direct cell-cell interactions. Elevated levels of circulating platelet-leukocyte aggregates are found in patients suffering from several thrombotic or inflammatory conditions. Platelet-monocyte and platelet-neutrophil interaction can trigger pro- and anti-inflammatory responses and modulate effector functions of all leukocyte subpopulations. These platelet-mediated immune responses have implications for the progression of cardiovascular diseases and also play a crucial role during infections, cancer, transplantations and other inflammatory diseases of several organs. Antiplatelet therapy including the COX inhibitor aspirin and/or ADP receptor P2Y12 inhibitors such as clopidogrel, prasugrel and ticagrelor are the therapy of choice for various cardiovascular complications. Both aspirin and P2Y12 inhibitors attenuate platelet-leukocyte interactions, thereby also modulating immune responses. This may have beneficial effects in some pathological conditions, while it might be detrimental in others. This review aims to summarise the current knowledge on platelet-leukocyte interactions and the impact of aspirin and P2Y12 inhibition on platelet-mediated immune responses and to give an overview on the effects of antiplatelet therapy on platelet-leukocyte interplay in various diseases.
authors.forename: Waltraud C
authors.initials: WC
authors.lastname: Schrottmaier
authors.forename: Julia B
authors.initials: JB
authors.lastname: Kral
authors.forename: Sigrun
authors.initials: S
authors.lastname: Badrnya
authors.affiliation: Dr. Alice Assinger, Centre for Physiology and Pharmacology, Medical University of Vienna, Schwarzspanierstrasse 17, A-1090 Vienna, Austria, Tel.: +43 1 40160 31405, E-mail: alice.assinger@meduniwien.ac.at.
authors.forename: Alice
authors.initials: A
authors.lastname: Assinger
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001241:Aspirin / Q000627:therapeutic use*; D001792:Blood Platelets / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D002450:Cell Communication / Q000187:drug effects*; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy* / Q000276:immunology; D018836:Inflammation Mediators / Q000097:blood; D009000:Monocytes / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D018375:Neutrophil Activation / Q000187:drug effects*; D009504:Neutrophils / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D058921:Purinergic P2Y Receptor Antagonists / Q000627:therapeutic use*; D058925:Receptors, Purinergic P2Y12 / Q000187:drug effects* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators; C548576:P2RY12 protein, human; D010975:Platelet Aggregation Inhibitors; D058921:Purinergic P2Y Receptor Antagonists; D058925:Receptors, Purinergic P2Y12; D001241:Aspirin
keywords: P2Y12 inhibitors; Platelet-leukocyte interaction; antiplatelet agents; aspirin; inflammation; platelet immunology