| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Outline of Final Research Achievements |
In the present study, we used a mouse model of sepsis and a model of neutrophil NETs formation to elucidate the role of the platelet-activated receptor CLEC-2 in the pathogenesis of sepsis. As a result, the survival rate due to platelet CLEC-2 expression in the sepsis model differed in the induction method. Induction by appendectomy significantly prolonged survival with CLEC-2 deficiency, but no difference was observed with LPS administration. In neutrophil NETs formation, co-culture with LPS and platelets induced NETs formation and was further inhibited by CLEC-2 blockers. This indicates that platelet CLEC-2 contributes to the formation of neutrophil NETs, which are involved in innate immunity.
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