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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.
Highlights
Influenza infection increases the incidence of myocardial infarction but the reason is unknown
This DNA co-localized with the neutrophil markers CD66b and myeloperoxidase (MPO) (Supplementary Fig. 2b, c), suggesting the possibility that the released DNA is due to NETosis
A possible reason for the discrepancy between released DNA observed by microscopy and lack of DNA detection in the plasma is that the platelet–neutrophil aggregates are large and spin down with cell fractions in blood
Summary
Influenza infection increases the incidence of myocardial infarction but the reason is unknown. 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 lead to thrombotic vascular occlusion. Heart disease is the leading cause of morbidity and mortality in the US with 735,000 people per year experiencing myocardial infarction (MI)[1] Viral infections such as influenza increase the incidence of acute MI within the first 7 days after detection of influenza A or B, whereas no increased incidence is observed after day 72. It is unclear if downstream activation of the immune system mediated by platelet-TLR7 leads to platelet-dependent thrombosis, which could potentially increase the risk for MI
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