Megakaryocytes and Platelets in Immune and Inflammatory Responses and in COVID-19

Update item information
Identifier megakaryocytes_and_platelets_in_immune_and_inflammatory_responses_and_in_COVID-19
Title Megakaryocytes and Platelets in Immune and Inflammatory Responses and in COVID-19
Creator Campbell, R., Rondina, M. U of U Health Key Faculty Collaborators: Schwertz, H., Rowley, J., Bray, P., Zimmerman, G., Weyrich, A., Middleton, E., Petrey, A., Con Yost, C.; Family and Preventive Medicine, Internal Medicine, Pathology, Pediatrics; School of Medicine, University of Utah Health
Subject Diffusion of Innovation; COVID-19; Inflammation; Megakaryocytes; Blood Platelets; Antiviral Agents; Thrombosis; Blood Coagulation; Mutation; Knowledge Discovery
Keyword Immunology, Inflammation, Infectious Disease
Image Caption Viral Infections Alter Megakaryocyte and Platelet Gene Expression and Function. SARS-CoV-2 infection generations thromboinflammatory agonists which alter platelet gene expression and function to promote increased platelet-leukocyte aggregates and platelet reactivity (Blood 2020).
Description Platelets-small cells which circulate in abundance in the bloodstream-are traditionally known for their ability to form clots and stop bleeding. Recent studies, however, have shown that platelets and their parent cells, megakaryocytes, also play a role in inflammation and infection. University of Utah Health investigators Robert Campbell, PhD, and Matthew Rondina, MD, and colleagues discovered that platelets and megakaryocytes respond robustly to infection, including COVID-19. These infection-driven changes in platelets activate clotting mechanisms and thus may contribute to the blood clots that complicate COVID-19 infection. Interestingly, Campell and Rondina and their collaborators also found that platelets and megakaryocytes demonstrate robust anti-viral defense properties that inhibit the spread of infection. Therefore, megakaryocytes from patients with genetic mutations in these anti-viral defense proteins are more susceptible to infection. These findings helped identify new pathways that regulate host responses to viral infection, and platelets are now being targeted therapeutically in patients with COVID-19.
Relation is Part of 2020
Publisher Spencer S. Eccles Health Sciences Library, University of Utah
Date Digital 2021
Date 2020
Type Image
Format image/jpeg
Rights Management Copyright © 2021, University of Utah, All Rights Reserved
Language eng
ARK ark:/87278/s6bp624d
References 1.) Human megakaryocytes possess intrinsic antiviral immunity through regulated induction of IFITM3. Campbell RA, Schwertz H, Hottz ED, Rowley JW, Manne BK, Washington AV, Hunter-Mellado R, Tolley ND, Christensen M, Eustes AS, Montenont E, Bhatlekar S, Ventrone CH, Kirkpatrick BD, Pierce KK, Whitehead SS, Diehl SA, Bray PF, Zimmerman GA, Kosaka Y, Bozza PT, Bozza FA, Weyrich AS, Rondina MT. Blood. 2019 May 9;133(19):2013-2026. 2.) Platelet gene expression and function in COVID-19 patients. Manne BK, Denorme F, Middleton EA, Portier I, Rowley JW, Stubben CJ, Petrey AC, Tolley ND, Guo L, Cody MJ, Weyrich AS, Yost CC, Rondina MT, Campbell RA. Blood. 2020 Sep 10;136(11):1317-1329. 3.) COVID-19 patients exhibit reduced procoagulant platelet responses. Denorme F, Manne BK, Portier I, Petrey AC, Middleton EA, Kile BT, Rondina MT, Campbell RA. J Thromb Haemost. 2020 Nov;18(11):3067-3073.
Press Releases and Media University of Utah Health "COVID-19 Causes ‘Hyperactivity' in Blood-clotting Cells,"; KUTV; KSL; Fox News; Reuters:; Newsweek:; Science Daily
Setname ehsl_50disc
ID 1697479
Reference URL