Thromb Haemost 2015; 114(03): 478-789
DOI: 10.1160/TH14-11-0943
Theme Issue Article
Schattauer GmbH

Aspirin and P2Y12 Inhibitors in platelet-mediated activation of neutrophils and monocytes

Waltraud C. Schrottmaier
1   Centre for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria
,
Julia B. Kral
1   Centre for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria
,
Sigrun Badrnya
1   Centre for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria
,
Alice Assinger
1   Centre for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria
2   Centre for Molecular Medicine, Department of Medicine, Karolinska University Hospital, Stockholm, Sweden
› Author Affiliations
Financial support: This study was supported by the Austrian Science Fund (FWF-P24978 and FWFSFB-54) and by the funding agency of the Austrian National Bank (OeNB grant 15961).
Further Information

Publication History

Received: 14 November 2014

Accepted after minor revision: 28 February 2015

Publication Date:
21 November 2017 (online)

Summary

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.

 
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