Analysis of gut microbiota and gut immunity in the development of IgA nephropathy using its mouse model
| Project/Area Number |
15K14360
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Laboratory animal science
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
成瀬 智恵 京都大学, 医学研究科, 助教 (30372486)
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| Co-Investigator(Renkei-kenkyūsha) |
SUGIHARA Kazushi 京都大学, 大学院医学研究科, 技術職員 (10377418)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | IgA腎症 / 糖鎖 / 腸内細菌叢 / 腸内細菌 |
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| Outline of Final Research Achievements |
β4GalT-1 KO mice that we generated spontaneously develop IgA nephropathy. To elucidate the mechanisms of IgA nephropathy in the mice, we examined gut microbiota, IgA producing cells in peripheral lymphoid tissues, distribution of blood cells in the gut and mucin-type carbohydrates. Whereas any significant differences were not observed in gut microbiota population between β4GalT-1 KO and control mice, the increase of IgA producing cells in peripheral lymphoid tissues, especially in mesenteric lymphnodes. Furthermore, B cells were accumulated in gut adhesive regions, suggesting these results might contribute hyper IgA in β4GalT-1 KO mice. Our project to generate IgA producing cell-specific or intestinal epithelial cell-specific conditional β4GalT-1 KO mice progressed to obtain ES cells in which a β4GalT-1 flox vector was knocked in.
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Report
(4 results)
Research Products
(3 results)
