| Project/Area Number |
17K17043
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Emergency medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 敗血症 / 免疫抑制 / 腹膜炎 / 虚血再灌流傷害 / 免疫調整 / 腸管虚血再還流 / 肺炎 / 腸管虚血再灌流 / 免疫賦活療法 / インターフェロンβ / 緑膿菌 / 肺胞マクロファージ / ARDS |
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| Outline of Final Research Achievements |
Assuming sepsis due to nosocomial pneumonia after peritonitis, we investigated the effect of interferon β administration on a two-hit animal model that causes Pseudomonas aeruginosa pneumonia after cecal ligation and puncture. Peritonitis made pneumonia more severe, and interferon β showed a therapeutic effect. In addition, the phagocytic ability of alveolar macrophages before pneumonia was evaluated, and peritonitis reduced the phagocytic ability, and interferon β restored the phagocytic ability. In addition, assuming ischemia-reperfusion due to shock or surgery, the survival rate and multi-organ damage of an animal model of intestinal ischemia-reperfusion injury were evaluated as the first hit. It was confirmed that the prolongation of the ischemic time made the disease more severe and that multiple organ damage was caused by intestinal ischemia-reperfusion.
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| Academic Significance and Societal Importance of the Research Achievements |
臨床では腹膜炎、肺炎などそれ自体であれば軽症であっても、それが組み合わさることで敗血症がより重症化することは多い。本検討ではそのような状況を想定したtwo hit動物モデルに対して、その重症化のメカニズムと治療薬としてインターフェロンβの効果を検討することで、敗血症の病態把握につながる結果としての意義がある。また同様に虚血再還流による多臓器障害やその免疫機能に与える影響を検討することで、その後の侵襲による重症化に与える影響を検討することは同じく敗血症の重症化のメカニズム解析につながる。
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