Early SARS-CoV-2 infection: Platelet-neutrophil complexes and platelet function

Rieder, Marina; Baldus, Niklas; Stallmann, Daniela; Jeserich, Maren; Goller, Isabella; Wirth, Luisa; Pollmeier, Luisa; Hofmann, Maike; Bode, Christoph; Busch, Hans-Joerg; Schmid, Bonaventura; Gauchel, Nadine; Scharf, Rüdiger E.; Duerschmied, Daniel; Lother, Achim; Krauel, Krystin

doi:10.1016/j.rpth.2022.100025

Cited by 4 publications

(5 citation statements)

References 52 publications

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“…Previously, it was shown that Mac-1 interacts with platelet glycoprotein Iba (vWF receptor) in mediating thrombosis (21, 85). Increased expression of both CD11b and CD18 on neutrophils isolated from COVID-19 patients was noted when compared to healthy volunteers suggesting one potential mechanism of platelet activation via Mac-1 binding of platelet GP Ib (43,45). Additionally, the behavior of three different neutrophil subpopulations in COVID-19 patients was investigated by Reyes et al First, neutrophils isolated by density gradient centrifugation from both the PMN and PBMC layer were separated into NDNs Graphical illustration of platelet-neutrophil interaction in COVID-19.…”

Section: Mac-1mentioning

confidence: 97%

“…As a side note, neutrophils contribute to CAC by releasing a variety of immune mediators causing a cytokine storm and DIC The first quantifiable endpoint of platelet and neutrophil interaction in CAC is represented by complex formation. As mentioned, such platelet-neutrophil aggregates (PNAs) are abundant in SARS-CoV-2 positive patients (37,41,45,(75)(76)(77). COVID-19 disease severity correlates with blood levels of PNAs (78).…”

Section: The Role Of Neutrophils and Nets In Cacmentioning

confidence: 99%

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Platelet-neutrophil interaction in COVID-19 and vaccine-induced thrombotic thrombocytopenia

Hirsch¹,

Uzun²,

Zlamal³

et al. 2023

Front. Immunol.

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Coronavirus disease 2019 (COVID-19) is known to commonly induce a thrombotic diathesis, particularly in severely affected individuals. So far, this COVID-19-associated coagulopathy (CAC) has been partially explained by hyperactivated platelets as well as by the prothrombotic effects of neutrophil extracellular traps (NETs) released from neutrophils. However, precise insight into the bidirectional relationship between platelets and neutrophils in the pathophysiology of CAC still lags behind. Vaccine-induced thrombotic thrombocytopenia (VITT) is a rare autoimmune disorder caused by auto-antibody formation in response to immunization with adenoviral vector vaccines. VITT is associated with life-threatening thromboembolic events and thus, high fatality rates. Our concept of the thrombophilia observed in VITT is relatively new, hence a better understanding could help in the management of such patients with the potential to also prevent VITT. In this review we aim to summarize the current knowledge on platelet-neutrophil interplay in COVID-19 and VITT.

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Section: Mac-1mentioning

confidence: 97%

Section: The Role Of Neutrophils and Nets In Cacmentioning

confidence: 99%

Platelet-neutrophil interaction in COVID-19 and vaccine-induced thrombotic thrombocytopenia

Hirsch¹,

Uzun²,

Zlamal³

et al. 2023

Front. Immunol.

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“…However, in recent studies, platelets from COVID-19 patients were shown to exhibit impaired aggregation and impaired activation of the responsible integrin receptor αIIbβ3 (GPIIb-IIIa) upon agonist-induced stimulation in vitro [ 56 , 57 ]. The reduced responsiveness of platelet functions ex vivo was not due to prior platelet activation in vivo.…”

Section: Pathogenesis Of Post-covid Syndromementioning

confidence: 99%

“…The reduced responsiveness of platelet functions ex vivo was not due to prior platelet activation in vivo. Interestingly, in one of the studies, a significantly increased proportion of circulating platelet-neutrophil conjugates was reported [ 56 ]. This observation reflects the interplay between platelets and neutrophils which is mediated by binding of platelet GPIbα to the MAC1 receptor (integrin αMβ2) on neutrophils.…”

Section: Pathogenesis Of Post-covid Syndromementioning

confidence: 99%

Post-COVID Syndrome in Adults—An Overview

Scharf

Anaya²

2023

Viruses

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This article provides an overview of various aspects related to post-COVID syndrome. Apart from its prevalence, symptoms and sequelae, risk determinants, and psychosocial implications, the pathogenesis of post-COVID condition is discussed in more detail. A focus on thrombo-inflammation in SARS-CoV-2 infection, the role of neutrophil extracellular traps, and the prevalence of venous thromboembolism is made. Moreover, COVID-19 and post-COVID syndrome in immunocompromising conditions, and the impact of vaccination on the prevention and treatment of post-COVID symptoms are reviewed. Autoimmunity is a hallmark of post-COVID syndrome, and, therefore, is another focus of this article. Thus, misdirected cellular and humoral immune responses can enhance the risk of latent autoimmunity in post-COVID syndrome. Facing the high prevalence of COVID-19 cases worldwide, it can be assumed that autoimmune disorders will increase globally over the next few years. Recent advances in identifying genetically determined variants may open the avenue for a better understanding of the susceptibility to and severity of SARS-CoV-2 infection and post-COVID syndrome.

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“…In line with this, impaired GPIIb/IIIa activation and reduced platelet aggregation have been shown in patients with alcoholic liver cirrhosis in response to stimulation in vitro [ 27 ]. Dysfunctional GPIIb/IIIa responses have been recently described for COVID-19 and sepsis [ 28 , 29 , 30 ]. However, except for one diagnosed dual hepatitis B/C virus infection, the patients included in this study had no other suspected or proven infection.…”

Section: Discussionmentioning

confidence: 99%

Decreased Platelet Aggregation in Patients with Decompensated Liver Cirrhosis and TIPS Implantation

et al. 2023

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Transjugular intrahepatic portosystemic shunt (TIPS) implantation is an effective treatment of portal hypertension in patients with decompensated liver cirrhosis. However, some patients develop TIPS thrombosis with recurrence of portal hypertension. The role of platelets in TIPS thrombosis and the necessity of antiplatelet therapy is unclear. Therefore, we aimed to study platelet function in patients with liver cirrhosis prior to and after TIPS implantation. Platelet aggregation was tested in peripheral and portal-vein blood patient samples on the day (D) of TIPS implantation (D0), D4 and D30 following the procedure (platelet count above 100 × 103/µL, aspirin starting on D5) using whole-blood impedance aggregometry (WBIA) and light transmission aggregometry (LTA). In addition, surface platelet activation markers (P-selectin, activated GPIIb/IIIa) and platelet–neutrophil complexes (PNCs) were assessed by flow cytometry. Thrombin receptor activating peptide 6 (TRAP-6), adenosine diphosphate (ADP) and arachidonic acid (AA) were used as agonists. Healthy subjects were included as controls. Agonist-induced platelet aggregation was reduced (WBIA: TRAP-6 p < 0.01, ADP p < 0.01, AA p < 0.001; LTA: TRAP-6 p = 0.13, ADP p = 0.05, AA p < 0.01) in patients (D0, n = 13) compared with healthy subjects (n = 9). While surface activation markers at baseline were negligibly low, the percentage of PNCs was higher in patients than in controls (p < 0.05). ADP-induced P-selectin expression was increased (p < 0.001), whereas TRAP-6-induced GPIIb/IIIa activation was impaired (p < 0.001) in patients versus controls. PNC formation in response to agonists was not different between groups. Results did not differ between peripheral and portal-vein blood of patients (D0, n = 11) and did not change over time (D0, D4, D30) following TIPS implantation (n = 9). In summary, patients with decompensated liver cirrhosis display in vitro platelet aggregation defects in response to various agonists. Defective aggregation persists upon TIPS implantation. Therefore, we conclude that antiplatelet treatment to prevent TIPS thrombosis is questionable.

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Early SARS-CoV-2 infection: Platelet-neutrophil complexes and platelet function

Cited by 4 publications

References 52 publications

Platelet-neutrophil interaction in COVID-19 and vaccine-induced thrombotic thrombocytopenia

Platelet-neutrophil interaction in COVID-19 and vaccine-induced thrombotic thrombocytopenia

Post-COVID Syndrome in Adults—An Overview

Decreased Platelet Aggregation in Patients with Decompensated Liver Cirrhosis and TIPS Implantation

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