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Article ; Online: Coagulation and complement: Key innate defense participants in a seamless web.

Pryzdial, Edward L G / Leatherdale, Alexander / Conway, Edward M

2022 Volume 13, Page(s) 918775

Abstract: In 1969, Dr. Oscar Ratnoff, a pioneer in delineating the mechanisms by which coagulation is activated and complement is regulated, wrote, "In the study of biological processes, the accumulation of information is often accelerated by a narrow point of ... ...

Abstract	In 1969, Dr. Oscar Ratnoff, a pioneer in delineating the mechanisms by which coagulation is activated and complement is regulated, wrote, "In the study of biological processes, the accumulation of information is often accelerated by a narrow point of view. The fastest way to investigate the body's defenses against injury is to look individually at such isolated questions as how the blood clots or how complement works. We must constantly remind ourselves that such distinctions are man-made. In life, as in the legal cliché, the devices through which the body protects itself form a seamless web, unwrinkled by our artificialities." Our aim in this review, is to highlight the critical molecular and cellular interactions between coagulation and complement, and how these two major component proteolytic pathways contribute to the seamless web of innate mechanisms that the body uses to protect itself from injury, invading pathogens and foreign surfaces.
MeSH term(s)	Blood Coagulation ; Cell Communication ; Complement System Proteins/metabolism ; Humans ; Thrombosis
Chemical Substances	Complement System Proteins (9007-36-7)
Language	English
Publishing date	2022-08-09
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.918775
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Complement contributions to COVID-19.

Conway, Edward M / Pryzdial, Edward L G

Current opinion in hematology

2022 Volume 29, Issue 5, Page(s) 259–265

Abstract: Purpose of review: COVID-19 remains a major source of concern, particularly as new variants emerge and with recognition that patients may suffer long-term effects. Mechanisms underlying SARS-CoV-2 mediated organ damage and the associated vascular ... ...

Abstract	Purpose of review: COVID-19 remains a major source of concern, particularly as new variants emerge and with recognition that patients may suffer long-term effects. Mechanisms underlying SARS-CoV-2 mediated organ damage and the associated vascular endotheliopathy remain poorly understood, hindering new drug development. Here, we highlight selected key concepts of how the complement system, a major component of innate immunity that is dysregulated in COVID-19, participates in the thromboinflammatory response and drives the vascular endotheliopathy. Recent findings: Recent studies have revealed mechanisms by which complement is activated directly by SARS-CoV-2, and how the system interfaces with other innate thromboinflammatory cellular and proteolytic pathways involving platelets, neutrophils, neutrophil extracellular traps and the coagulation and kallikrein-kinin systems. With this new information, multiple potential sites for therapeutic intervention are being uncovered and evaluated in the clinic. Summary: Infections with SARS-CoV-2 cause damage to the lung alveoli and microvascular endothelium via a process referred to as thromboinflammation. Although not alone in being dysregulated, complement is an early player, prominent in promoting the endotheliopathy and consequential organ damage, either directly and/or via the system's complex interplay with other cellular, molecular and biochemical pathways. Delineating these critical interactions is revealing novel and promising strategies for therapeutic intervention.
MeSH term(s)	COVID-19 ; Complement System Proteins ; Extracellular Traps ; Humans ; Inflammation ; SARS-CoV-2 ; Thrombosis/etiology
Chemical Substances	Complement System Proteins (9007-36-7)
Language	English
Publishing date	2022-07-11
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1153887-9
ISSN	1531-7048 ; 1065-6251
ISSN (online)	1531-7048
ISSN	1065-6251
DOI	10.1097/MOH.0000000000000724
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Zs.A 3703: Show issues

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Article ; Online: Maestro tissue factor reaches new hEIGHT.

Pryzdial, Edward L G

Blood

2017 Volume 130, Issue 14, Page(s) 1604–1605

MeSH term(s)	Factor VIII ; Humans ; Thromboplastin
Chemical Substances	Factor VIII (9001-27-8) ; Thromboplastin (9035-58-9)
Language	English
Publishing date	2017-10-04
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2017-08-798520
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Zs.MO 364: Show issues

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Article ; Online: Thrombotic triad in microgravity.

Elahi, Mohammad M / Witt, Alexandra N / Pryzdial, Edward L G / McBeth, Paul B

Thrombosis research

2023 Volume 233, Page(s) 82–87

Abstract: Thrombotic disease may be an underdiagnosed condition of prolonged exposure to microgravity and yet the underlying factors remain poorly defined. Recently, an internal jugular vein thrombosis was diagnosed in a low-risk female astronaut after an ... ...

Abstract	Thrombotic disease may be an underdiagnosed condition of prolonged exposure to microgravity and yet the underlying factors remain poorly defined. Recently, an internal jugular vein thrombosis was diagnosed in a low-risk female astronaut after an approximately 7-week space mission. Six of the additional 10 crew members demonstrated jugular venous flow risk factors, such as suspicious stagnation or retroversion. Fortunately, all were asymptomatic. Observations in space as well as clinical and in vitro microgravity studies on Earth, where experiments are designed to recapitulate the conditions of space, suggest effects on blood flow stasis, coagulation, and vascular function. In this article, the related literature on thrombotic disease in space is reviewed, with consideration of these elements of Virchow's triad.
MeSH term(s)	Humans ; Female ; Weightlessness/adverse effects ; Thrombosis ; Blood Coagulation ; Jugular Veins ; Hemodynamics
Language	English
Publishing date	2023-11-22
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	121852-9
ISSN	1879-2472 ; 0049-3848
ISSN (online)	1879-2472
ISSN	0049-3848
DOI	10.1016/j.thromres.2023.11.020
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Zs.A 863: Show issues

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Article ; Online: Correction of haemorrhagic shock-associated coagulopathy and impaired haemostasis by plasma, prothrombin complex concentrates or an activated protein C-targeted DNA aptamer in mice.

Eltringham-Smith, Louise J / Meixner, Scott C / Pryzdial, Edward L G / Sheffield, William P

Scientific reports

2023 Volume 13, Issue 1, Page(s) 3811

Abstract: Even with extensive transfusion support, trauma-induced bleeding often leads to death. Early intervention may improve outcomes, yet which blood products, factor concentrates, or other drugs constitute optimal treatment is unclear. Patients with acute ... ...

Abstract	Even with extensive transfusion support, trauma-induced bleeding often leads to death. Early intervention may improve outcomes, yet which blood products, factor concentrates, or other drugs constitute optimal treatment is unclear. Patients with acute traumatic coagulopathy (ATC), arising from trauma and haemorrhagic shock, have the worst prognosis. Here, multiple interventions were compared in a mouse model of ATC. After the trauma of tissue excision, anaesthetized mice were bled to 35 mm Hg mean arterial pressure, maintained under shock for 60 min, and resuscitated with fluids equal in volume to the shed blood. Resuscitated mice were subjected to liver laceration to test haemostasis and blood loss was quantified. Saline-treated mice lost two- to three-fold more blood than sham-treated animals and were coagulopathic by prothrombin time elevation post- versus pre-procedure. Murine fresh-frozen plasma (mFFP), anti-activated protein C aptamer HS02-52G, or prothrombin complex concentrates eliminated the bleeding diathesis and coagulopathy; fibrinogen, plasminogen activator inhibitor-1, or tranexamic acid ameliorated bleeding or coagulopathy, but not both. HS02-52G and mFFP also eliminated the changes in plasma aPC and tissue plasminogen activator levels observed in saline-treated mice, as judged via microtiter plate biomarker assays. Procoagulant interventions, especially inhibiting aPC, could be beneficial in human ATC.
Language	English
Publishing date	2023-03-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-30794-7
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Article ; Online: Is the COVID-19 thrombotic catastrophe complement-connected?

Conway, Edward M / Pryzdial, Edward L G

Journal of thrombosis and haemostasis : JTH

2020 Volume 18, Issue 11, Page(s) 2812–2822

Abstract: In December 2019, the world was introduced to a new betacoronavirus, referred to as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) for its propensity to cause rapidly progressive lung damage, resulting in high death rates. As fast as the ... ...

Abstract	In December 2019, the world was introduced to a new betacoronavirus, referred to as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) for its propensity to cause rapidly progressive lung damage, resulting in high death rates. As fast as the virus spread, it became evident that the novel coronavirus causes a multisystem disease (COVID-19) that may involve multiple organs and has a high risk of thrombosis associated with striking elevations in pro-inflammatory cytokines, D-dimer, and fibrinogen, but without disseminated intravascular coagulation. Postmortem studies have confirmed the high incidence of venous thromboembolism, but also notably revealed diffuse microvascular thrombi with endothelial swelling, consistent with a thrombotic microangiopathy, and inter-alveolar endothelial deposits of complement activation fragments. The clinicopathologic presentation of COVID-19 thus parallels that of other thrombotic diseases, such as atypical hemolytic uremic syndrome (aHUS), that are caused by dysregulation of the complement system. This raises the specter that many of the thrombotic complications arising from SARS-CoV-2 infections may be triggered and/or exacerbated by excess complement activation. This is of major potential clinical relevance, as currently available anti-complement therapies that are highly effective in protecting against thrombosis in aHUS, could be efficacious in COVID-19. In this review, we provide mounting evidence for complement participating in the pathophysiology underlying the thrombotic diathesis associated with pathogenic coronaviruses, including SARS-CoV-2. Based on current knowledge of complement, coagulation and the virus, we suggest lines of study to identify novel therapeutic targets and the rationale for clinical trials with currently available anti-complement agents for COVID-19.
MeSH term(s)	Animals ; Anticoagulants/therapeutic use ; Blood Coagulation/drug effects ; COVID-19/blood ; COVID-19/immunology ; COVID-19/virology ; Complement Activation/drug effects ; Complement Inactivating Agents/therapeutic use ; Complement System Proteins/immunology ; Host-Pathogen Interactions ; Humans ; SARS-CoV-2/immunology ; Thrombosis/blood ; Thrombosis/immunology ; Thrombosis/prevention & control ; Thrombosis/virology ; COVID-19 Drug Treatment
Chemical Substances	Anticoagulants ; Complement Inactivating Agents ; Complement System Proteins (9007-36-7)
Keywords	covid19
Language	English
Publishing date	2020-09-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1111/jth.15050
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Zs.A 5805: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Is the COVID‐19 thrombotic catastrophe complement‐connected?

Conway, Edward M. / Pryzdial, Edward L. G.

Journal of Thrombosis and Haemostasis ; ISSN 1538-7933 1538-7836

2020

Keywords	Hematology ; covid19
Language	English
Publisher	Wiley
Publishing country	us
Document type	Article ; Online
DOI	10.1111/jth.15050
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Antiviral anticoagulation.

Pryzdial, Edward L G / Sutherland, Michael R / Lin, Bryan H / Horwitz, Marc

Research and practice in thrombosis and haemostasis

2020 Volume 4, Issue 5, Page(s) 774–788

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel envelope virus that causes coronavirus disease 2019 (COVID-19). Hallmarks of COVID-19 are a puzzling form of thrombophilia that has elevated D-dimer but only modest effects on other ... ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel envelope virus that causes coronavirus disease 2019 (COVID-19). Hallmarks of COVID-19 are a puzzling form of thrombophilia that has elevated D-dimer but only modest effects on other parameters of coagulopathy. This is combined with severe inflammation, often leading to acute respiratory distress and possible lethality. Coagulopathy and inflammation are interconnected by the transmembrane receptor, tissue factor (TF), which initiates blood clotting as a cofactor for factor VIIa (FVIIa)-mediated factor Xa (FXa) generation. TF also functions from within the nascent TF/FVIIa/FXa complex to trigger profound changes via protease-activated receptors (PARs) in many cell types, including SARS-CoV-2-trophic cells. Therefore, aberrant expression of TF may be the underlying basis of COVID-19 symptoms. Evidence suggests a correlation between infection with many virus types and development of clotting-related symptoms, ranging from heart disease to bleeding, depending on the virus. Since numerous cell types express TF and can act as sites for virus replication, a model envelope virus, herpes simplex virus type 1 (HSV1), has been used to investigate the uptake of TF into the envelope. Indeed, HSV1 and other viruses harbor surface TF antigen, which retains clotting and PAR signaling function. Strikingly, envelope TF is essential for HSV1 infection in mice, and the FXa-directed oral anticoagulant apixaban had remarkable antiviral efficacy. SARS-CoV-2 replicates in TF-bearing epithelial and endothelial cells and may stimulate and integrate host cell TF, like HSV1 and other known coagulopathic viruses. Combined with this possibility, the features of COVID-19 suggest that it is a TFopathy, and the TF/FVIIa/FXa complex is a feasible therapeutic target.
Keywords	covid19
Language	English
Publishing date	2020-07-06
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2475-0379
ISSN (online)	2475-0379
DOI	10.1002/rth2.12406
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Article: Is the COVID-19 thrombotic catastrophe complement-connected?

Conway, Edward M / Pryzdial, Edward L G

J. thromb. haemost

Abstract	In December 2019, the world was introduced to a new betacoronavirus, referred to as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) for its propensity to cause rapidly progressive lung damage, resulting in high death rates. As fast as the virus spread, it became evident that the novel coronavirus causes a multisystem disease (COVID-19) that may involve multiple organs and has a high risk of thrombosis associated with striking elevations in pro-inflammatory cytokines, D-dimer, and fibrinogen, but without disseminated intravascular coagulation. Postmortem studies have confirmed the high incidence of venous thromboembolism, but also notably revealed diffuse microvascular thrombi with endothelial swelling, consistent with a thrombotic microangiopathy, and inter-alveolar endothelial deposits of complement activation fragments. The clinicopathologic presentation of COVID-19 thus parallels that of other thrombotic diseases, such as atypical hemolytic uremic syndrome (aHUS), that are caused by dysregulation of the complement system. This raises the specter that many of the thrombotic complications arising from SARS-CoV-2 infections may be triggered and/or exacerbated by excess complement activation. This is of major potential clinical relevance, as currently available anti-complement therapies that are highly effective in protecting against thrombosis in aHUS, could be efficacious in COVID-19. In this review, we provide mounting evidence for complement participating in the pathophysiology underlying the thrombotic diathesis associated with pathogenic coronaviruses, including SARS-CoV-2. Based on current knowledge of complement, coagulation and the virus, we suggest lines of study to identify novel therapeutic targets and the rationale for clinical trials with currently available anti-complement agents for COVID-19.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #697181
Database	COVID19

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Article: Spotlight on animal models of acute traumatic coagulopathy: an update.

Ask, Antje / Eltringham-Smith, Louise / Bhakta, Varsha / Donkor, David A / Pryzdial, Edward L G / Sheffield, William P

Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis

2022 Volume 61, Issue 2, Page(s) 103412

Abstract: Critically injured persons suffer trauma, hemorrhage, and high mortality. A subset of such patients develops early coagulation dysfunction characterized as acute traumatic coagulopathy (ATC), with a poor prognosis. The mechanisms contributing to ATC ... ...

Abstract	Critically injured persons suffer trauma, hemorrhage, and high mortality. A subset of such patients develops early coagulation dysfunction characterized as acute traumatic coagulopathy (ATC), with a poor prognosis. The mechanisms contributing to ATC remain incompletely understood. Notwithstanding some successes in conducting clinical trials in early traumatic coagulopathy, conducting clinical research in ATC is ethically and logistically challenging. In vitro studies cannot capture the complex pathophysiological interplay between blood, vasculature, and organ systems relevant to ATC. Animal models are therefore vital for understanding ATC and to test interventions. Previous systematic reviews of animal models of ATC covered progress up to 2014. The current review aimed to extend that coverage to the end of 2021. A structured systematic search of MEDLINE/PubMed was carried out and identified 56 relevant publications. Unlike in previous reviews, where pig models predominated, rat and pig models contributed equally (19 studies each), and non-human primate models entered the field. Most studies now featured defined trauma (39 of 56), and hemorrhage controlled by pressure or volume (42 studies), with some documenting that both were necessary to induce ATC. Most studies documented coagulopathy using clotting or viscoelastometric assays and created an endogenous coagulopathy not dependent on iatrogenic dilution. As before, the diversity of species and experimental protocols may limit the translatability of the identified studies. Thus, while animal research has become more aligned to clinical realities since 2014, further efforts are required to unravel ATC mechanisms and enable the prediction and evaluation of optimal clinical interventions.
MeSH term(s)	Animals ; Blood Coagulation ; Blood Coagulation Disorders/etiology ; Disease Models, Animal ; Hemorrhage ; Humans ; Rats ; Swine ; Wounds and Injuries/complications
Language	English
Publishing date	2022-03-10
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2046795-3
ISSN	1878-1683 ; 1473-0502
ISSN (online)	1878-1683
ISSN	1473-0502
DOI	10.1016/j.transci.2022.103412
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