ArticleBlood2018
Peptidoglycan induces disseminated intravascular coagulation in baboons through activation of both coagulation pathways.
Article in Blood, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 37 citations in OpenAlex.
- Anthrax toxins exacerbate sepsis-induced coagulopathy and endothelial dysfunction in a baboon model of anthrax.Journal of thrombosis and haemostasis : JTH · 2026Article
- Bacterial infection and activation of the contact pathway of coagulation.Blood vessels, thrombosis & hemostasis · 2025Review
- Protective effects of factor XI inhibition by abelacimab in a baboon model of live Staphylococcus aureus sepsis.Journal of thrombosis and haemostasis : JTH · 2025Article
- Novel insights into the association between organ damage and inflammatory response in preoperative abdominal aortic aneurysms.Frontiers in cardiovascular medicine · 2025Article
- The physicochemical properties of lipopolysaccharide chemotypes regulate activation of the contact pathway of blood coagulation.The Journal of biological chemistry · 2025Article
- Monocyte uptake of polymeric peptidoglycan is bimodal and governed by complement C3 and C4 opsonins.JCI insight · 2024Article
- Peptidoglycan from Bacillus anthracis Inhibits Human Macrophage Efferocytosis in Part by Reducing Cell Surface Expression of MERTK and TIM-3.ImmunoHorizons · 2024Article
- Circulating LPS from gut microbiota leverages stenosis-induced deep vein thrombosis in mice.Thrombosis journal · 2023Article
- Gram-Positive Bacteria Cell Wall Peptidoglycan Polymers Activate Human Dendritic Cells to Produce IL-23 and IL-1β and Promote TMicroorganisms · 2023Article
- Article
- Internalization of Polymeric Bacterial Peptidoglycan Occurs through Either Actin or Dynamin Dependent Pathways.Microorganisms · 2022Article
- Altered fibrin clot structure and dysregulated fibrinolysis contribute to thrombosis risk in severe COVID-19.Blood advances · 2022Article
- A potential new pathway for heparin treatment of sepsis-induced lung injury: inhibition of pulmonary endothelial cell pyroptosis by blocking hMGB1-LPS-induced caspase-11 activation.Frontiers in cellular and infection microbiology · 2022Review
- Complement C5 inhibition protects against hemolytic anemia and acute kidney injury in anthrax peptidoglycan-induced sepsis in baboons.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Detailed exploration of pathophysiology involving inflammatory status and bleeding symptoms between lipopolysaccharide- and tissue factor-induced disseminated intravascular coagulation in rats.International journal of hematology · 2021Article
- Article
- A Review of the Efficacy of FDA-ApprovedToxins · 2021Review
- Hypercoagulation detected by routine and global laboratory hemostasis assays in patients with infective endocarditis.PloS one · 2021Observational
- Hydrocortisone decreases lethality and inflammatory cytokine and nitric oxide production in rats challenged with B. anthracis cell wall peptidoglycan.Intensive care medicine experimental · 2020Article
- The role of endothelial shear stress on haemodynamics, inflammation, coagulation and glycocalyx during sepsis.Journal of cellular and molecular medicine · 2020Review
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Anthrax infections exhibit progressive coagulopathies that may contribute to the sepsis pathophysiology observed in fulminant disease. The hemostatic imbalance is recapitulated in primate models of late-stage disease but is uncommon in toxemic models, suggesting contribution of other bacterial pathogen-associated molecular patterns (PAMPs). Peptidoglycan (PGN) is a bacterial PAMP that engages cellular components at the cross talk between innate immunity and hemostasis. We hypothesized that PGN is critical for anthrax-induced coagulopathies and investigated the activation of blood coagulation in response to a sterile PGN infusion in primates. The PGN challenge, like the vegetative bacteria, induced a sepsis-like pathophysiology characterized by systemic inflammation, disseminated intravascular coagulation (DIC), organ dysfunction, and impaired survival. Importantly, the hemostatic impairment occurred early and in parallel with the inflammatory response, suggesting direct engagement of coagulation pathways. PGN infusion in baboons promoted early activation of contact factors evidenced by elevated protease-serpin complexes. Despite binding to contact factors, PGN did not directly activate either factor XII (FXII) or prekallikrein. PGN supported contact coagulation by enhancing enzymatic function of active FXII (FXIIa) and depressing its inhibition by antithrombin. In parallel, PGN induced de novo monocyte tissue factor expression in vitro and in vivo, promoting extrinsic clotting reactions at later stages. Activation of platelets further amplified the procoagulant state during PGN challenge, leading to DIC and subsequent ischemic damage of peripheral tissues. These data indicate that PGN may be a major cause for the pathophysiologic progression of
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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.