RGD Reference Report - Activated protein C ameliorates Bacillus anthracis lethal toxin-induced lethal pathogenesis in rats. - Rat Genome Database

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Activated protein C ameliorates Bacillus anthracis lethal toxin-induced lethal pathogenesis in rats.

Authors: Kau, JH  Shih, YL  Lien, TS  Lee, CC  Huang, HH  Lin, HC  Sun, DS  Chang, HH 
Citation: Kau JH, etal., J Biomed Sci. 2012 Nov 21;19:98. doi: 10.1186/1423-0127-19-98.
RGD ID: 11100034
Pubmed: PMID:23170801   (View Abstract at PubMed)
PMCID: PMC3536616   (View Article at PubMed Central)
DOI: DOI:10.1186/1423-0127-19-98   (Journal Full-text)

BACKGROUND: Lethal 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. METHODS: To 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. RESULTS: Fibrin 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. CONCLUSIONS: These 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.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
PROCHumanEndotoxemia treatmentIDA  RGD 
ProcRatEndotoxemia treatmentISOPROC (Homo sapiens) RGD 
ProcMouseEndotoxemia treatmentISOPROC (Homo sapiens) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Proc  (protein C, inactivator of coagulation factors Va and VIIIa)

Genes (Mus musculus)
Proc  (protein C)

Genes (Homo sapiens)
PROC  (protein C, inactivator of coagulation factors Va and VIIIa)


Additional Information