ArticleJournal of biomedical science2012
Activated protein C ameliorates Bacillus anthracis lethal toxin-induced lethal pathogenesis in rats.
Article in Journal of biomedical science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
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- P-Selectin is a Critical Factor for Platelet-Mediated Protection on Restraint Stress-Induced Gastrointestinal Injury in Mice.International journal of molecular sciences · 2022Article
- Thioacetamide-induced liver damage and thrombocytopenia is associated with induction of antiplatelet autoantibody in mice.Scientific reports · 2019Article
- TRPM8 and RAAS-mediated hypertension is critical for cold-induced immunosuppression in mice.Oncotarget · 2018Article
- Soluble P-selectin rescues mice from anthrax lethal toxin-induced mortality through PSGL-1 pathway-mediated correction of hemostasis.Virulence · 2017Article
- Antibacterial Properties of Visible-Light-Responsive Carbon-Containing Titanium Dioxide Photocatalytic Nanoparticles against Anthrax.Nanomaterials (Basel, Switzerland) · 2016Article
- Soluble P-selectin rescues viper venom-induced mortality through anti-inflammatory properties and PSGL-1 pathway-mediated correction of hemostasis.Scientific reports · 2016Article
- Nanodiamonds protect skin from ultraviolet B-induced damage in mice.Journal of nanobiotechnology · 2015Article
- Acquired coagulant factor VIII deficiency induced by Bacillus anthracis lethal toxin in mice.Virulence · 2015Article
- Anti-inflammatory functions of protein C require RAGE and ICAM-1 in a stimulus-dependent manner.Mediators of inflammation · 2014Article
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- Targeting the host hemostatic system function in bacterial infection for antimicrobial therapies.Journal of thrombosis and thrombolysis · 2014Review
- Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLethal toxin (LT) is a major virulence factor of Bacillus anthracis. Sprague Dawley rats manifest pronounced lung edema and shock after LT treatments, resulting in high mortality. The heart failure that is induced by LT has been suggested to be a principal mechanism of lung edema and mortality in rodents. Since LT-induced death occurs more rapidly in rats than in mice, suggesting that other mechanisms in addition to the heart dysfunction may be contributed to the fast progression of LT-induced pathogenesis in rats. Coagulopathy may contribute to circulatory failure and lung injury. However, the effect of LT on coagulation-induced lung dysfunction is unclear.
methodsTo investigate the involvement of coagulopathy in LT-mediated pathogenesis, the mortality, lung histology and coagulant levels of LT-treated rats were examined. The effects of activated protein C (aPC) on LT-mediated pathogenesis were also evaluated.
resultsFibrin depositions were detected in the lungs of LT-treated rats, indicating that coagulation was activated. Increased levels of plasma D-dimer and thrombomodulin, and the ameliorative effect of aPC further suggested that the activation of coagulation-fibrinolysis pathways plays a role in LT-mediated pathogenesis in rats. Reduced mortality was associated with decreased plasma levels of D-dimer and thrombomodulin following aPC treatments in rats with LT-mediated pathogenesis.
conclusionsThese findings suggest that the activation of coagulation in lung tissue contributes to mortality in LT-mediated pathogenesis in rats. In addition, anticoagulant aPC may help to develop a feasible therapeutic strategy.
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