| Project/Area Number |
15H06176
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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 |
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) |
2015-08-28 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| 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 | 敗血症 / ARDS / インターフェロンβ / マクロファージ |
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| Outline of Final Research Achievements |
We evaluate effects of IFNb in a murine model of septic pneumonia. Murine sepsis was induced by cecal ligation and puncture (CLP). Pneumonia was made with instillation of Pseudomonas aeruginosa. Outcomes included survival, lung histology, cytokine responses in blood and lung, alveolar macrophage (AM) phagocytosis. While mortality from sepsis or pneumonia alone was low, pneumonia following sepsis resulted in increased mortality in association with an altered profile of blood/alveolar cytokines, reduced alveolar macrophage localization of neutrophils into the endoalveolar space. IFNb normalized alveolar macrophage phagocytic function and neutrophil chemoattractant release, and improved survival in a murine model of pneumonia following sepsis. Impaired host defense mechanism might associate with higher mortality in septic pneumonia mouse model. Subcutaneous IFNb may restore production of inflammatory cytokines in the lung and impaired alveolar macrophage functions.
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