| Project/Area Number |
23500958
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Eating habits, studies on eating habits
|
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KATAOKA Keiko 徳島大学, ヘルスバイオサイエンス研究部, 教授 (40189303)
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| Co-Investigator(Kenkyū-buntansha) |
ARIMOCHI Hideki 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 助教 (30311822)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 腸内菌 / 無菌マウス / ノトバイオートマウス / B細胞 / インターロイキンー１０ / インターロイキンー２２ / 大腸炎モデル / インターロイキン-10 |
|---|
| Research Abstract |
We searched intestinal bacteria which can induce interleukin-10-producing cells. B cell-like cell population in mucosa of mouse small intestine was very little under germ free condition, but increased age-dependently or by administration of SPF mice feces. This cell population was decreased by antibiotics for Gram-positive bacteria, and increased in mice monoassociated with Enterococcus, an Gram-positive bacteria. This population additionally produced interleukin-22 which can mediate the production of antibacterial peptide and tissue repair. Partially purified fraction of this population showed inhibitory effect on colitis in naive T cell-transferred mice, and the effect was cancelled by injection of anti-interleukin-10 antibody.
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