Mechanisms of Immunothrombosis by SARS-CoV-2

Hernández-Huerta, María Teresa; Pérez-Santiago, Alma Dolores; Mayoral, Eduardo Pérez-Campos; Navarro, Luis Manuel Sánchez; Canales, Francisco Javier Rodal; Majluf‐Cruz, Abraham; Matías-Cervantes, Carlos Alberto; Mayoral, Eduardo Pérez-Campos; Díaz, Carlos Romero; Andrade, Gabriel Mayoral; Cruz, Margarito Martínez; Ángel, Judith Luna; Pérez-Campos, Eduardo

doi:10.3390/biom11111550

Cited by 13 publications

(11 citation statements)

References 137 publications

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“…[7]. One explanation for vascular thrombi in the background of COVID-19 could be related to the angiotensin-converting enzyme 2 (ACE2) receptor and cytokine storms [8,9]. The binding and activation of the ACE2 receptor will cause damage to endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…Falasca et al reported a series of 22 autopsies on decedents with severe COVID-19 infection and demonstrated prominent microvascular damage and thrombosis [ 7 ]. One explanation for vascular thrombi in the background of COVID-19 could be related to the angiotensin-converting enzyme 2 (ACE2) receptor and cytokine storms [ 8 , 9 ]. The binding and activation of the ACE2 receptor will cause damage to endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…The binding and activation of the ACE2 receptor will cause damage to endothelial cells. The disruption of the ACE2 receptor by the virus then causes an imbalance in the ACE2 axis, which induces the cytokine IL-6, TNF-a storm, and other inflammatory responses [ 8 , 9 ]. Subsequentially, this activates the coagulation cascade and the platelet response, which eventually induces thrombotic effects throughout the body [ 10 ].…”

Section: Discussionmentioning

confidence: 99%

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A Series of COVID-19 Cases With Findings in the Gastrointestinal and Hepatobiliary System

Dong-ling¹,

Hacking²,

Lee³

2022

Cureus

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Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly spread worldwide. Most of the infected patients present with respiratory symptoms and acute lung damage. Here, we present three cases of patients with COVID-19 disease whose main clinical manifestations are gastrointestinal symptoms. In our first case, we present a COVID-19 patient with histologic findings associated with ischemic necrosis of the small bowel. In the second and third cases, we demonstrate acute cholecystitis and histology showing microvascular thrombosis. These three cases highlight the ischemic and thrombotic changes seen in the setting of COVID-19 infection without classic respiratory symptoms, with resulting severe gastrointestinal and hepatobiliary disease requiring surgical management. Although the bile or stool viral load was not tested in these patients, the small intestine and gallbladder were infected with SARS-CoV-2, most likely via the epithelial angiotensin-converting enzyme 2 (ACE2) receptor.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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A Series of COVID-19 Cases With Findings in the Gastrointestinal and Hepatobiliary System

Dong-ling¹,

Hacking²,

Lee³

2022

Cureus

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“…NETs, damage-associated molecular patterns, oxygen radicals, and many other factors are involved in this pathway. 17 In the SARS-CoV-2 specific pathway, the reaction is initiated by the binding of virus spike protein to its receptor. SARS-CoV-2 infects host cells by binding spike protein to angiotensin-converting enzyme 2 (ACE2), expressed on alveolar epithelial cells, enterocytes, monocytes/macrophages, platelets, and vascular endothelial cells.…”

Section: Platelet Activation In Covid-19mentioning

confidence: 99%

Platelet Activation and Thrombosis in COVID-19

Iba

Wada

Levy

2022

Semin Thromb Hemost

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Although thrombosis frequently occurs in infectious diseases, the coagulopathy associated with COVID-19 has unique characteristics. Compared with bacterial sepsis, COVID-19-associated coagulopathy presents with minimal changes in platelet counts, normal prothrombin times, and increased D-dimer and fibrinogen levels. These differences can be explained by the distinct pathophysiology of the thromboinflammatory responses. In sepsis-induced coagulopathy, leukocytes are primarily responsible for the coagulopathy by expressing tissue factor, releasing neutrophil extracellular traps, multiple procoagulant substances, and systemic endothelial injury that is often associated with vasoplegia and shock. In COVID-19-associated coagulopathy, platelet activation is a major driver of inflammation/thrombogenesis and von Willebrand factor and platelet factor 4 are deeply involved in the pathogenesis. Although the initial responses are localized to the lung, they can spread systemically if the disease is severe. Since the platelets play major roles, arterial thrombosis is not uncommon in COVID-19. Despite platelet activation, platelet count is usually normal at presentation, but sensitive biomarkers including von Willebrand factor activity, soluble P-selectin, and soluble C-type lectin-like receptor-2 are elevated, and they increase as the disease progresses. Although the role of antiplatelet therapy is still unproven, current studies are ongoing to determine its potential effects.

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“…Platelets also express proteins, which if localized in the extracellular milieu and possibly conveyed by pEVs, may stimulate inflammation due to molecular profiles. These molecules, known as damage-associated molecular patterns (DAMPs), include highmobility group box 1 (HMGB1) and calprotectin (S100A8/9), which have been identified in numerous inflammatory conditions such as systemic sclerosis, systemic lupus erythematosus, and COVID-19 [122][123][124][125][126][127].…”

mentioning

confidence: 99%

Platelet extracellular vesicles and the secretory interactome join forces in health and disease

Boilard

Bellio

2022

Immunological Reviews

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Summary Extracellular vesicles (EVs) are small membrane‐bound vesicles released by cells under various conditions. They are found in the extracellular milieu in all biological fluids. As the concentrations, contents, and origin of EVs can change during inflammation, the assessment of EVs can be used as a proxy of cellular activation. Here, we review the literature regarding EVs, more particularly those released by platelets and their mother cells, the megakaryocytes. Their cargo includes cytokines, growth factors, organelles (mitochondria and proteasomes), nucleic acids (messenger and non‐coding RNA), transcription factors, and autoantigens. EVs may thus contribute to intercellular communication by facilitating exchange of material between cells. EVs also interact with other molecules secreted by cells. In autoimmune diseases, EVs are associated with antibodies secreted by B cells. By definition, EVs necessarily comprise a phospholipid moiety, which is thus the target of secreted phospholipases also abundantly expressed in the extracellular milieu. We discuss how platelet‐derived EVs, which represent the majority of the circulating EVs, may contribute to immunity through the activity of their cargo or in combination with the secretory interactome.

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Mechanisms of Immunothrombosis by SARS-CoV-2

Cited by 13 publications

References 137 publications

A Series of COVID-19 Cases With Findings in the Gastrointestinal and Hepatobiliary System

A Series of COVID-19 Cases With Findings in the Gastrointestinal and Hepatobiliary System

Platelet Activation and Thrombosis in COVID-19

Platelet extracellular vesicles and the secretory interactome join forces in health and disease

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