| Project/Area Number |
15H06403
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
General internal medicine(including psychosomatic medicine)
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| Research Institution | Kobe University |
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Principal Investigator |
Shimizu Mami 神戸大学, 医学研究科, 医学研究員 (10757313)
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| Research Collaborator |
INOUE Yuto 神戸大学, 大学院保健学研究科
WAKAFUJI Ryo 神戸大学, 大学院保健学研究科
TAGAMI Kanako 神戸大学, 大学院保健学研究科
NISHIKAWA Minaho 神戸大学, 大学院保健学研究科
KATSUTA Atsumi 神戸大学, 大学院医学研究科, 研究助手
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| Project Period (FY) |
2015-08-28 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | １型糖尿病 / SR-A / 腸内細菌 / ＴＬＲ４ / 1型糖尿病 / TLR4 / スカベンジャー受容体 / TLR |
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| Outline of Final Research Achievements |
Recently, it has been reported that the development of type 1 diabetes would be associated with commensal bacteria. So the aim of this study was to examine the association between scavenger receptor A (SR-A) and Toll-like receptor 4 (TLR4) as a sensor of the gram-negative rod on dendritic cells and to establish a new immunological preventative and therapeutic strategy for type 1 diabetes. First, lipopolysaccharide (LPS) as a ligand of TLR4 was administered to female NOD mice and cyclophosphamide (CY) -induced diabetes model in male NOD mice. Second, LPS was administered to SR-A KO NOD mice and CY-induced diabetes model in SR-A KO NOD mice. As a result, LPS administration prevented diabetes onset in female NOD mice and CY-induce diabetes model in male NOD mice, but not in SR-A KO situations. Flow cytometric analysis suggested that the Foxp3 regulatory T cells might play a pivotal role in the mechanism of LPS tolerance.
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