Platelets and Immune Responses during Thromboinflammation
- 1University Heart Center Luebeck, Germany
- 2Clinic for Heart Surgery, University Hospital Erlangen, Germany
- 3University Medical Center Schleswig-Holstein, Germany
- 4Department of Cardiac and Thoracic Vascular Surgery, University Medical Center Schleswig-Holstein, Germany
Besides mediating hemostatic functions, platelets are increasingly recognized as important players involved in inflammation. Data from experiments in mice and men revealed various points of intersection between thrombosis, hemostasis and inflammation, which are addressed and discussed in this review in detail. One such example is the intrinsic coagulation cascade that is initiated after platelet activation thereby further propagating and re-enforcing wound healing or thrombus formation, which contributes to the pathophysiology of severe diseases. FXII of the intrinsic pathway connects platelet activation with the coagulation cascade during immune reactions. It can activate the contact system thereby either creating an inflammatory state or accelerating inflammation. Recent insights into platelet biology could show that platelets are equipped with complement receptors. Platelets are important for tissue remodeling after injury has been inflicted to the endothelial barrier and to the subendothelial tissue. Thus, platelets are increasingly recognized as more than just cells relevant for bleeding arrest or thrombus formation, and further interesting insights into platelet biology are to be discovered. In the future this understanding will potentially offer novel opportunities for therapeutic intervention in diseases, where platelets are involved.
Keywords: platelets, Inflammation, Atherosclerosis, Thrombosis, Immunity, innate immunity
Received: 15 Mar 2019;
Accepted: 09 Jul 2019.
Edited by:Benoît Ho-Tin-Noé, Institut National de la Santé et de la Recherche Médicale (INSERM), France
Reviewed by:Robert H. Lee, University of North Carolina at Chapel Hill, United States
Frederik Denorme, The University of Utah, United States
Copyright: © 2019 Mezger, Nording, Sauter, Graf, Heim, von Bubnoff, Ensminger and Langer. 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.
* Correspondence: Prof. Harald F. Langer, University Heart Center Luebeck, Lübeck, 23538, Germany, email@example.com