ArticleBlood advances2022
Platelet-monocyte interaction amplifies thromboinflammation through tissue factor signaling in COVID-19.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 71 citations in OpenAlex.
- Monocyte Activation Drives Atrial Fibrillation in Hypertension.Cardiovascular drugs and therapy · 2026Article
- Platelet homeostasis and heterogeneity in inflammation and sepsis: mechanisms, biological effects, and clinical potential.Cell communication and signaling : CCS · 2026Review
- Increased impact of GPIb receptors on platelet adhesion under flow in severe COVID-19.Biophysics reports · 2026Article
- Multiorgan Molecular Landscape of Severe COVID-19 Revealed by Consensus Gene Signatures and RAB8B Targeting.Journal of medical virology · 2026Article
- Platelet-driven monocyte activation promotes hypoxic thromboinflammation through the HIF-1α-NLRP3-EGR-1 axis.Haematologica · 2026Article
- P-Selectin and Platelet-Monocyte Interaction in Inflammation: Mechanisms, Hypothesis, and Open Questions.Journal of inflammation research · 2026Review
- Role of monocytes in the pathogenesis of antiphospholipid syndrome and potential therapeutic targets (Review).Molecular medicine reports · 2025Review
- Beyond hemostasis, the immunomodulatory nature of platelets.Research and practice in thrombosis and haemostasis · 2025Review
- Review
- Evaluation of the podoplanin/C-type lectin-like receptor-2 (CLEC-2) pathway as a mediator of platelet and coagulation activation in sickle cell disease.Research and practice in thrombosis and haemostasis · 2025Article
- Pattern recognition receptor-associated immuno-thrombotic transcript changes in platelets and leukocytes with COVID19.PLoS pathogens · 2025Article
- Dysregulation of immune cells and platelet-monocyte aggregates in chronic thromboembolic pulmonary hypertension.Respiratory research · 2025Article
- Imaging of Thromboinflammation by MultispectralInternational journal of molecular sciences · 2025Review
- Platelets Modulate Leukocyte Population Composition Within Perivascular Adipose Tissue.International journal of molecular sciences · 2025Article
- Activation of the Coagulation Cascade as a Universal Danger Sign.Current issues in molecular biology · 2025Review
- Dengue infection changes the expressions of CD154 and CD148 in human platelets.Virus research · 2025Article
- Complex Pattern of Platelet Activation/Reactivity After SARS-CoV-2 Infection.International journal of molecular sciences · 2024Review
- Association between mean platelet volume and adiponectin in patients with metabolic syndrome.Journal of applied biomedicine · 2024Article
- The differential formation and composition of leukocyte-platelet aggregates induced by various cellular stimulants.Thrombosis research · 2024Article
- Response by Goonewardena et al to Letter Regarding Article, "Monocyte-Mediated Thrombosis Linked to Circulating Tissue Factor and Immune Paralysis in COVID-19".Arteriosclerosis, thrombosis, and vascular biology · 2024Article
Corrections and comments
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Authors and funding
19 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence into the pathogenesis of COVID-19 highlights a hypercoagulability state with high risk of life-threatening thromboembolic complications. However, the mechanisms of hypercoagulability and their link to hyperinflammation remain poorly understood. Here, we investigate functions and mechanisms of platelet activation and platelet-monocyte interactions in inflammatory amplification during SARS-CoV-2 infection. We used a combination of immunophenotyping, single-cell analysis, functional assays, and pharmacological approaches to gain insights on mechanisms. Critically ill patients with COVID-19 exhibited increased platelet-monocyte aggregates formation. We identified a subset of inflammatory monocytes presenting high CD16 and low HLA-DR expression as the subset mainly interacting with platelets during severe COVID-19. Single-cell RNA-sequencing analysis indicated enhanced fibrinogen receptor Mac-1 in monocytes from patients with severe COVID-19. Monocytes from patients with severe COVID-19 displayed increased platelet binding and hyperresponsiveness to P-selectin and fibrinogen with respect to tumor necrosis factor-α and interleukin-1β secretion. Platelets were able to orchestrate monocyte responses driving tissue factor (TF) expression, inflammatory activation, and inflammatory cytokines secretion in SARS-CoV-2 infection. Platelet-monocyte interactions ex vivo and in SARS-CoV-2 infection model in vitro reciprocally activated monocytes and platelets, inducing the heightened secretion of a wide panel of inflammatory mediators. We identified platelet adhesion as a primary signaling mechanism inducing mediator secretion and TF expression, whereas TF signaling played major roles in amplifying inflammation by inducing proinflammatory cytokines, especially tumor necrosis factor-α and interleukin-1β. Our data identify platelet-induced TF expression and activity at the crossroad of coagulation and inflammation in severe COVID-19.
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