ReviewJournal of cellular and molecular medicine2012
Pathophysiology, staging and therapy of severe sepsis in baboon models.
Review in Journal of cellular and molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 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
- A stable systemic infection of methicillin-resistantFrontiers in microbiology · 2025Article
- Insights into pathophysiology and therapeutic strategies for heat stroke: Lessons from a baboon model.Experimental physiology · 2024Review
- Organotypic heterogeneity in microvascular endothelial cell responses in sepsis-a molecular treasure trove and pharmacological Gordian knot.Frontiers in medicine · 2023Review
- 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
- CD14 inhibition improves survival and attenuates thrombo-inflammation and cardiopulmonary dysfunction in a baboon model of Escherichia coli sepsis.Journal of thrombosis and haemostasis : JTH · 2021Article
- The Toll-Like Receptor 2 Ligand Pam2CSK4 Activates Platelet Nuclear Factor-κB and Bruton's Tyrosine Kinase Signaling to Promote Platelet-Endothelial Cell Interactions.Frontiers in immunology · 2021Article
- Fondaparinux pentasaccharide reduces sepsis coagulopathy and promotes survival in the baboon model of Escherichia coli sepsis.Journal of thrombosis and haemostasis : JTH · 2020Article
- Inhibition of contact-mediated activation of factor XI protects baboons againstBlood advances · 2019Article
- Nonhuman primate species as models of human bacterial sepsis.Lab animal · 2019Review
- Response patterns of routinely measured inflammatory and coagulatory parameters in sepsis.PeerJ · 2019Article
- Inflammatory and coagulatory parameters linked to survival in critically ill children with sepsis.Annals of intensive care · 2018Article
- Article
- In vivo-generated thrombin and plasmin do not activate the complement system in baboons.Blood · 2017Article
- Identification of key genes in Gram‑positive and Gram‑negative sepsis using stochastic perturbation.Molecular medicine reports · 2017Article
- Inhibition of complement C5 protects against organ failure and reduces mortality in a baboon model ofProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Sphingosine 1-phosphate and its carrier apolipoprotein M in human sepsis and in Escherichia coli sepsis in baboons.Journal of cellular and molecular medicine · 2016Article
- Could Biomarkers Direct Therapy for the Septic Patient?The Journal of pharmacology and experimental therapeutics · 2016Review
- Complement inhibition decreases early fibrogenic events in the lung of septic baboons.Journal of cellular and molecular medicine · 2015Article
- Crosstalk between the coagulation and complement systems in sepsis.Thrombosis research · 2014Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We review our baboon models of Escherichia coli sepsis that mimic, respectively, the shock/disseminated intravascular coagulation (DIC) and organ failure variants of severe sepsis, and analyse the pathophysiologic processes that are unique to each. The multi-stage, multi-factorial characteristics of severe sepsis develop as a result of the initial insult, which - depending on its intensity - activates components of the intravascular compartment leading to overwhelming shock/DIC; or initiates a sequence of events involving both the intra- and extravascular (tissues) compartments that lead to organ failure. In the latter case, the disorder passes through two stages: an initial inflammatory/coagulopathic intravascular first stage triggered by E. coli, followed by an extravascular second stage, involving components unique to each organ and triggered by ischemia/reperfusion (oxidative stress and histone release). Although a myriad of overlapping cellular and molecular components are involved, it is the context in which these components are brought into play that determine whether shock/DIC or organ failure predominate. For example, inflammatory and thrombotic responses amplified by thrombin in the first case whereas similar responses are amplified by complement activation products in the second. Rather than blocking specific mediators, we found that attenuation of the thrombin and complement amplification pathways can effectively reverse the shock/DIC and organ failure exhibited by the LD(100) and LD(50) E. coli models of severe sepsis, respectively. Translation of these concepts to successful intervention in the respective baboon models of E. coli sepsis and the application to their clinical counterparts is described.
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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.