| Project/Area Number |
19J10790
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| Research Category |
Grant-in-Aid for JSPS Fellows
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| Allocation Type | Single-year Grants |
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| Section | 国内 |
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| Review Section |
Basic Section 55010:General surgery and pediatric surgery-related
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| Research Institution | Osaka University |
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Principal Investigator |
李 波 大阪大学, 医学系研究科, 特別研究員(PD)
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| Project Period (FY) |
2019-04-25 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2020: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2019: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | E-NTPD8 / P2X4 / ATP / DSS-induced colitis / 壊死性腸炎 / 組換えヒト可溶性トロンボモジュリン（rTM） / ラットモデル |
|---|
| Outline of Research at the Start |
1). Generate gnotobiotic mice colonized with human breast milk fed preterm infant microbiota (HMb) or formula fed preterm infant microbiota (FMb).
2). Explore how HMb mice and FMb mice differ in susceptibility to NEC-like injury.
3). Reveal causal bacterial family associated with survival from NEC.
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| Outline of Annual Research Achievements |
新生児ラットモデルを用いて、壊死性腸炎に対して組換えヒト可溶性トロンボモジュリンは効果があることがわかりました。研究結果はSurgery Todayに掲載されました。その後腸管免疫に関する研究を行いました。
要約は以下の通りです。
We show that E-NTPD8 is highly expressed in large intestinal epithelial cells and hydrolyzes microbiota-derived luminal adenosine triphosphate ATP. Compared to wild-type mice, Entpd8-/- mice develop more severe DSS-induced colitis. In this context, either depletion of neutrophils and monocytes by injecting with anti-Gr-1 antibody or introduction of P2rx4 deficiency into hematopoietic cells relieve colitis in Entpd8-/- mice. Increased level of luminal ATP in the colon of Entpd8-/- mice promotes glycolysis in neutrophils and monocytes through P2X4 receptor-dependent Ca2+ influx, which links to prolonged survival and elevated ROS production in these cells.
今論文は投稿中です。
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| Research Progress Status |
令和2年度が最終年度であるため、記入しない。
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| Strategy for Future Research Activity |
令和2年度が最終年度であるため、記入しない。
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