ArticleClinical and experimental immunology2015
The key roles of complement and tissue factor in Escherichia coli-induced coagulation in human whole blood.
Article in Clinical and experimental immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Type 1 diabetes mellitus (T1DM) does not affect whole blood responses to alginate-based microspheres despite plasma lipid and glucose differences.Materials today. Bio · 2025Article
- Monocyte Tissue Factor Expression: Lipopolysaccharide Induction and Roles in Pathological Activation of Coagulation.Thrombosis and haemostasis · 2023Review
- Coagulopathy and thromboembolic events a pathogenic mechanism of COVID-19 associated with mortality: An updated review.Journal of clinical laboratory analysis · 2023Review
- MS-proteomics provides insight into the host responses towards alginate microspheres.Materials today. Bio · 2022Article
- Dysregulated miRNAs network in the critical COVID-19: An important clue for uncontrolled immunothrombosis/thromboinflammation.International immunopharmacology · 2022Review
- Interplay between inflammation and thrombosis in cardiovascular pathology.Nature reviews. Cardiology · 2021Review
- Bothrops lanceolatus snake (Fer-de-lance) venom triggers inflammatory mediators' storm in human blood.Archives of toxicology · 2021Article
- Complement Inhibition and COVID-19: The Story so Far.ImmunoTargets and therapy · 2021Review
- The Prothrombotic State Associated with SARS-CoV-2 Infection: Pathophysiological Aspects.Mediterranean journal of hematology and infectious diseases · 2021Review
- Is COVID-19 associated thrombosis caused by overactivation of the complement cascade? A literature review.Thrombosis research · 2020Review
- Alternative Complement Pathway Activation Provokes a Hypercoagulable State with Diminished Fibrinolysis.Shock (Augusta, Ga.) · 2020Article
- Does Complement-Mediated Hemostatic Disturbance Occur in Traumatic Brain Injury? A Literature Review and Observational Study Protocol.International journal of molecular sciences · 2020Review
- Heparin and non-anticoagulant heparin attenuate histone-induced inflammatory responses in whole blood.PloS one · 2020Article
- Cholesterol Crystals Induce Coagulation Activation through Complement-Dependent Expression of Monocytic Tissue Factor.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- The Release of Monocyte-Derived Tissue Factor-Positive Microparticles Contributes to a Hypercoagulable State in Idiopathic Membranous Nephropathy.Journal of atherosclerosis and thrombosis · 2019Article
- Complement component 5 does not interfere with physiological hemostasis but is essential for Escherichia coli-induced coagulation accompanied by Toll-like receptor 4.Clinical and experimental immunology · 2019Article
- Iron Dysregulation and Dormant Microbes as Causative Agents for Impaired Blood Rheology and Pathological Clotting in Alzheimer's Type Dementia.Frontiers in neuroscience · 2018Review
- Alginate microbeads are coagulation compatible, while alginate microcapsules activate coagulation secondary to complement or directly through FXII.Acta biomaterialia · 2017Article
- Article
- Dual inhibition of complement and Toll-like receptors as a novel approach to treat inflammatory diseases-C3 or C5 emerge together with CD14 as promising targets.Journal of leukocyte biology · 2017Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement system and the Toll-like (TLR) co-receptor CD14 play important roles in innate immunity and sepsis. Tissue factor (TF) is a key initiating component in intravascular coagulation in sepsis, and long pentraxin 3 (PTX3) enhances the lipopolysaccharide (LPS)-induced transcription of TF. The aim of this study was to study the mechanism by which complement and CD14 affects LPS- and Escherichia coli (E. coli)-induced coagulation in human blood. Fresh whole blood was anti-coagulated with lepirudin, and incubated with ultra-purified LPS (100 ng/ml) or with E. coli (1 × 10(7) /ml). Inhibitors and controls included the C3 blocking peptide compstatin, an anti-CD14 F(ab')2 antibody and a control F(ab')2 . TF mRNA was measured using quantitative polymerase chain reaction (qPCR) and monocyte TF surface expression by flow cytometry. TF functional activity in plasma microparticles was measured using an amidolytic assay. Prothrombin fragment F 1+2 (PTF1.2) and PTX3 were measured by enzyme-linked immunosorbent assay (ELISA). The effect of TF was examined using an anti-TF blocking antibody. E. coli increased plasma PTF1.2 and PTX3 levels markedly. This increase was reduced by 84->99% with compstatin, 55-97% with anti-CD14 and > 99% with combined inhibition (P < 0·05 for all). The combined inhibition was significantly (P < 0·05) more efficient than compstatin and anti-CD14 alone. The LPS- and E. coli-induced TF mRNA levels, monocyte TF surface expression and TF functional activity were reduced by > 99% (P < 0·05) with combined C3 and CD14 inhibition. LPS- and E. coli-induced PTF1.2 was reduced by 76-81% (P < 0·05) with anti-TF antibody. LPS and E. coli activated the coagulation system by a complement- and CD14-dependent up-regulation of TF, leading subsequently to prothrombin activation.
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