Anna Vogelsang - Department of Neurology with Institute of Translational Neurology, University of Muenster, Germany
Susann Eichler - Department of Neurology with Institute of Translational Neurology, University of Muenster, Germany
Sven G. Meuth - Department of Neurology with Institute of Translational Neurology, University of Muenster, Germany

Blood-brain-barrier disruption and immune cell infiltration are hallmarks of multiple sclerosis (MS) and experimental autoimmuneencephalomyelitis (EAE). Not only immune cells, but also platelets infiltrate the central nervous system (CNS) and accumulate in lesions during neuroinflammation. Inside lesions, degranulating platelets secrete inflammatory and vasoactive substances, which seem to promote immune cell infiltration. Recent studies demonstrated that depletion of platelets during the effector phase of EAE diminish gene expressions of intercellular-adhesion-molecule-1 (ICAM-1) and vascular-cell-adhesion-molecule-1 (VCAM-1) in CNS tissue1. However, a deeper understanding of the interplay between platelets and endothelial cells is required. Materials and Methods: Here, we examined the impactof platelet-derived releasate on brain microvascular endothelial cells. Therefore, platelets were either activated by thrombin or adenosine diphosphate (ADP). Then, primary endothelial cells treated with plateletderived releasates were analyzed for gene expressionsof cell-adhesion and tight-junction molecules. Results: Platelet-derived releasate generated with ADP leads on endothelial cells to a pronounced upregulation of ICAM- 1 (39.18-fold) and VCAM-1 (5.8-fold) that support diapedesis of immune cells. Whereas the stimulationwith thrombin mediates opposite effects. Conclusion: We conclude that different activation pathways seem to alter the proinflammatory activity of platelets. However, further investigations are needed to elucidate the underlying mechanisms of platelet activation and itsimpact on neuroinflammation.