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Complement component 5 promotes lethal thrombosis.
Tomohiro Mizuno1, Kengo Yoshioka1, Masashi Mizuno2
1Department of Analytical Pharmacology, Meijo University, Nagoya, Japan.
Scientific Reports
|February 17, 2017
Summary
Complement component 5 (C5) exacerbates histone-induced lethal thrombosis and liver injury. C5-deficient mice showed protection against thrombosis, coagulopathy, and liver damage, highlighting C5
Area of Science:
- Immunology
- Hematology
- Hepatology
Background:
- Extracellular histones trigger platelet aggregation and thrombosis, leading to coagulation factor depletion.
- Complement component 5 (C5) is implicated in platelet aggregation and coagulation activation.
- The precise mechanisms of histone-induced liver injury remain incompletely understood.
Purpose of the Study:
- To investigate the role of C5 in promoting liver injury during histone-induced lethal thrombosis.
- To elucidate the pathological pathways linking C5, thrombosis, and liver damage.
Main Methods:
- C5-sufficient and C5-deficient mice were intravenously injected with calf thymus histones.
- Survival rates were monitored for 72 hours.
- Blood cell counts, liver function, coagulation, platelet aggregation, and platelet/leukocyte aggregate (PLA) production were analyzed.
Main Results:
- C5-deficient mice exhibited significantly improved survival compared to C5-sufficient mice.
- Reduced thrombocytopenia, consumptive coagulopathy, and liver injury with embolism were observed in C5-deficient mice.
- Lower PLA production was noted in C5-deficient mice, indicating reduced inflammatory response.
Conclusions:
- C5 plays a critical role in the pathogenesis of lethal thrombosis and associated liver injury induced by extracellular histones.
- C5 contributes to coagulation disorders, PLA formation, and embolism-induced liver damage.
- Targeting C5 may offer a therapeutic strategy for mitigating histone-induced thrombotic events and organ injury.
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