Presentation Details
| Platelet immunophenotype induced by the Spike (S) protein and the RBD domain of SARS-CoV-2 virus. Alan Cano-Mendez, Nallely Garcia-Larragoiti, Yesenia Ambriz-Murillo, Patricia Guzman-Cansino, Alejandra Ochoa-Zarzosa, Martha Eva Viveros-Sandoval. Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Mexico |
Abstract
Background: COVID-19 caused by SARS-CoV-2 has affected millions of people worldwide. This viral agent uses the Spike (S) protein to infect target cells. An active immunothrombotic state has been described in severe stages of infection. Platelets are cells involved in the inflammatory and thrombotic process and have been positioned as immune system sentinel cells due to their unique characteristics. Aim: To study the platelet immunophenotype induced by the complete Spike protein and the RBD domain of SARS-CoV-2 virus. Methodology: Blood samples were obtained from healthy volunteers by venipuncture after signing an informed consent form. 3.2% sodium citrate was used as anticoagulant. Platelet-rich plasma (PRP) was obtained by slow centrifugation (100 g x 10 minutes). PRP was separated and resuspended in Tyrodes. Stimulation of PRP (1X107 cells/ml) with protein S and protein S receptor binding domain (RBD) [2 ug/ml] was performed for different times, 37°C. A panel of inflammatory biomarkers was analyzed by flow cytometry using the LEGENDplex Kit TM Human Thrombosis Panel Standard BioLegend® and the LEGENDplex Kit TM Human Innflammation Panel 1 Standard BioLegend® (San Diego, CA, USA) following the instructions suggested by the supplier. Results: The complete Spike protein and the RBD domain induce platelet expression of factors that contribute to the inflammatory process. We observed that cells treated with the protein secrete concentrations of IL-6, IL-8, INF- α2, IL-1B and IL-10 when compared to the expression of these factors in untreated PRP or upon stimulation with vehicle (p<0.05) and with procoagulant agonists such as ADP, epinephrine and collagen. Conclusion: Protein S and the RBD domain induce a proinflammatory phenotype in platelets, favoring the perpetuation of the immunothrombotic environment.
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No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.