A mouse model of sepsis-associated DIC induced by Kappa-carrageenan and Lipopolysaccharides: Establishment and characteristics.

Summary

Combining kappa-carrageenan (100 mg/kg) with LPS (50 μg/kg) produced tail thrombosis, prolonged aPTT, hypocoagulability, and time-resolved inflammation and fibrinolysis inhibition, stabilizing by 12 hours with thrombi in tail, lung, and liver. Lower ambient temperature exacerbated thrombosis, and strain differences were defined (KM/BALB/c > ICR). This standardized model recapitulates key clinical-pathological features of sepsis-associated DIC.

Key Findings

• Optimal KCG (100 mg/kg) + LPS (50 μg/kg) dosing induced tail thrombosis, prolonged aPTT, and hypocoagulability.
• Ambient temperature at 16±1°C worsened thrombosis and hypocoagulability versus 24±1°C; sex had similar responses.
• Time course showed early fibrinolysis inhibition (<1 h), evolving inflammation/ coagulopathy (1.5–24 h), and organ thrombi (tail, lung, liver) with dysfunction by 12 h; strain differences observed (KM/BALB/c > ICR).

Clinical Implications

Although preclinical, this model can accelerate evaluation of anticoagulant, antifibrinolytic, and anti-inflammatory interventions tailored to sepsis-associated DIC.

Limitations

• Mouse model may not fully capture human DIC heterogeneity and comorbidities
• Therapeutic interventions were not tested within this report

Future Directions

Apply the model to evaluate anticoagulants, fibrinolytics, and immunomodulators; integrate omics to map coagulation–inflammation networks.