| Project/Area Number |
16570112
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional biochemistry
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| Research Institution | Kanazawa University |
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Principal Investigator |
SHIRATSUCHI Akiko Kanazawa Univ., Grad.Sch.Med.Sci., Assistant Professor, 医学系研究科, 講師 (90303297)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2004: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | phagocytosis / innate immuniti / phosphatidylserine / spermatogenesis / influenza virus / scavenger receptor / insect immunity |
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| Research Abstract |
1) Mechanism and role of SR-BI-mediated apoptotic spermatogenic cells by Sertoli cells in the testis
After binding of phosphatidylserine on the surface of apoptotic cells, SR-BI in Sertoli cells induces phhosphorylation of MAP kinase p38 and ERKI/II. In the presence of inhibitors for p38-pathway and ERK-pathway, phagocytosis of apoptotic cells by Sertoli cells was inhibited greatly. These results showed that SR-BI, when it binds to phosphatidylserine, transmits signals to activate MAP kinase pathway, which leads to the induction of the engulfment of phosphatidylserine-exposing apoptotic cells by phagocytic cells.
2) Role of phagocytosis of ineluenza virus-infected cells by phagocytes
In the lung of influenza virus-infected mice, virus-infected cells were shown in both neutrophils and alveolar macrophages. Administration of the phagocytosis inhibitors into the lung caused both the lethality in mice and the extent of inflammation in the lung were augmented in those mice. These results suggest that phagocytosis of virus-infected cells helps suppress the progress of influenza in mice.
3) Regulation of phagosome-lysosome fusion
MAP kinase p38-pathway and ERK-pathway were activated in macrophages after incubation with apoptotic cells, and the activity seemed to be needed to phagosome-lysosome fusion in macrophages.
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