The role of platelets in mediating a response to human influenza infection

Milka Koupenova (), Heather A. Corkrey, Olga Vitseva, Giorgia Manni, Catherine J. Pang, Lauren Clancy, Chen Yao, Jeffrey Rade, Daniel Levy, Jennifer P. Wang, Robert W. Finberg, Evelyn A. Kurt-Jones and Jane E. Freedman
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Milka Koupenova: Division of Cardiovascular Medicine
Heather A. Corkrey: Division of Cardiovascular Medicine
Olga Vitseva: Division of Cardiovascular Medicine
Giorgia Manni: University of Perugia
Catherine J. Pang: University of Massachusetts Medical School
Lauren Clancy: Division of Cardiovascular Medicine
Chen Yao: National Institutes of Health
Jeffrey Rade: Division of Cardiovascular Medicine
Daniel Levy: National Institutes of Health
Jennifer P. Wang: University of Massachusetts Medical School
Robert W. Finberg: University of Massachusetts Medical School
Evelyn A. Kurt-Jones: University of Massachusetts Medical School
Jane E. Freedman: Division of Cardiovascular Medicine

Nature Communications, 2019, vol. 10, issue 1, 1-18

Abstract: Abstract Influenza infection increases the incidence of myocardial infarction but the reason is unknown. Platelets mediate vascular occlusion through thrombotic functions but are also recognized to have immunomodulatory activity. To determine if platelet processes are activated during influenza infection, we collected blood from 18 patients with acute influenza infection. Microscopy reveals activated platelets, many containing viral particles and extracellular-DNA associated with platelets. To understand the mechanism, we isolate human platelets and treat them with influenza A virus. Viral-engulfment leads to C3 release from platelets as a function of TLR7 and C3 leads to neutrophil-DNA release and aggregation. TLR7 specificity is confirmed in murine models lacking the receptor, and platelet depletion models support platelet-mediated C3 and neutrophil-DNA release post-influenza infection. These findings demonstrate that the initial intrinsic defense against influenza is mediated by platelet–neutrophil cross-communication that tightly regulates host immune and complement responses but can also lead to thrombotic vascular occlusion.

Date: 2019
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DOI: 10.1038/s41467-019-09607-x

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