ArticleBlood2010
Complement inhibition decreases the procoagulant response and confers organ protection in a baboon model of Escherichia coli sepsis.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
117 citing papers in PubMed, 181 citations in OpenAlex.
- Thirty-Eight-Negative Kinase 1 Is a Mediator of Acute Kidney Injury in Experimental and Clinical Traumatic Hemorrhagic Shock.Frontiers in immunology · 2020Trial
- The Effect of Esmolol on Tissue Perfusion and Clinical Prognosis of Patients with Severe Sepsis: A Prospective Cohort Study.BioMed research international · 2016Trial
- Lipopolysaccharide and Coagulation Factor XII: Biophysics of Contact Activation in Infection.Seminars in thrombosis and hemostasis · 2026Review
- Integrative metabolite-protein interaction networks reveal potential pathways and biomarkers in sepsis.BMC infectious diseases · 2026Article
- Modes of (Inter)Actions of Polyvalent Immunoglobulins: Nonclinical and Clinical Research in Severe Bacterial Infections.Biomedicines · 2026Review
- Anthrax toxins exacerbate sepsis-induced coagulopathy and endothelial dysfunction in a baboon model of anthrax.Journal of thrombosis and haemostasis : JTH · 2026Article
- Functional Roles of the Complement Immune System in Cardiac Inflammation and Hypertrophy.International journal of molecular sciences · 2025Review
- The dysfunction of complement and coagulation in diseases: the implications for the therapeutic interventions.MedComm · 2024Review
- Complement system activation: bridging physiology, pathophysiology, and therapy.Intensive care medicine · 2024Review
- Understanding, assessing and treating immune, endothelial and haemostasis dysfunctions in bacterial sepsis.Intensive care medicine · 2024Review
- Pathophysiological dynamics in the contact, coagulation, and complement systems during sepsis: Potential targets for nafamostat mesilate.Journal of intensive medicine · 2024Review
- Dysregulation of Host-Pathogen Interactions in Sepsis: Host-Related Factors.Seminars in respiratory and critical care medicine · 2024Review
- Navigating the Modern Landscape of Sepsis: Advances in Diagnosis and Treatment.International journal of molecular sciences · 2024Review
- Complement networks in gene-edited pig xenotransplantation: enhancing transplant success and addressing organ shortage.Journal of translational medicine · 2024Review
- Unraveling the Intricate Web: Complement Activation Shapes the Pathogenesis of Sepsis-Induced Coagulopathy.Journal of innate immunity · 2024Review
- Targeting the host response in sepsis: current approaches and future evidence.Critical care (London, England) · 2023Review
- Glomerular injury after trauma, burn, and sepsis.Journal of nephrology · 2023Review
- Review
- Complement System Inhibitory Drugs in a Zebrafish (International journal of molecular sciences · 2023Article
- Sepsis: network pathophysiology and implications for early diagnosis.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Review
57 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Severe sepsis leads to massive activation of coagulation and complement cascades that could contribute to multiple organ failure and death. To investigate the role of the complement and its crosstalk with the hemostatic system in the pathophysiology and therapeutics of sepsis, we have used a potent inhibitor (compstatin) administered early or late after Escherichia coli challenge in a baboon model of sepsis-induced multiple organ failure. Compstatin infusion inhibited sepsis-induced blood and tissue biomarkers of complement activation, reduced leucopenia and thrombocytopenia, and lowered the accumulation of macrophages and platelets in organs. Compstatin decreased the coagulopathic response by down-regulating tissue factor and PAI-1, diminished global blood coagulation markers (fibrinogen, fibrin-degradation products, APTT), and preserved the endothelial anticoagulant properties. Compstatin treatment also improved cardiac function and the biochemical markers of kidney and liver damage. Histologic analysis of vital organs collected from animals euthanized after 24 hours showed decreased microvascular thrombosis, improved vascular barrier function, and less leukocyte infiltration and cell death, all consistent with attenuated organ injury. We conclude that complement-coagulation interplay contributes to the progression of severe sepsis and blocking the harmful effects of complement activation products, especially during the organ failure stage of severe sepsis is a potentially important therapeutic strategy.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.