ArticleJournal of thrombosis and haemostasis : JTH2026
Anthrax toxins exacerbate sepsis-induced coagulopathy and endothelial dysfunction in a baboon model of anthrax.
Article in Journal of thrombosis and haemostasis : JTH, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
backgroundAnthrax, caused by Bacillus anthracis, leads to severe sepsis due to multiple virulence factors, including toxins and bacterial cell wall components, which disrupt immune responses and induce cytotoxic effects. However, the relative contributions of toxins vs bacterial overload during systemic disease remain unclear.
objectivesWe aimed to investigate the differential effects of toxigenic B anthracis Sterne strains and nontoxigenic ΔSterne strains on coagulation, complement activation, immune response, endothelial function, and organ damage in a baboon model of anthrax.
methodsHealthy baboons were intravenously infused with a sublethal dose (1 × 10
resultsThe toxigenic Sterne strain induced more severe systemic effects than the ΔSterne strain, including prolonged bacterial persistence, enhanced coagulopathy, increased complement activation, endothelial dysfunction, neutrophil activation, and neutrophil extracellular trap formation. Coagulopathy was evidenced by elevated protease-antithrombin complexes, prolonged clotting times, fibrinogen consumption, and thrombocytopenia. Proteomic analysis of plasma revealed stronger upregulation of proteins involved in innate immunity, metabolism, coagulation, and cell death pathways in Sterne animals compared with ΔSterne-challenged animals.
conclusionOur findings suggest that anthrax toxins contribute to the exacerbation of pathological host responses during anthrax sepsis, including coagulopathy, complement activation, endothelial dysfunction, and organ injury. These observations provide insight into the role of toxins in intensifying disease severity beyond bacterial burden alone. Therapeutic strategies targeting coagulation and complement pathways, while preserving endothelial function, may help mitigate anthrax-induced sepsis.
Indexed as
Identifiers
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.