| Project/Area Number |
18K08898
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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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| Review Section |
Basic Section 55060:Emergency medicine-related
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| Research Institution | Saitama Medical University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2020: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2019: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 敗血症 / 急性炎症 / IL6 signaling / 臓器障害 / 低体温 / 肺障害 / IL-6 signaling / 臓器保護 |
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| Outline of Final Research Achievements |
Using the cecal ligation and puncture (CLP)-incduced septic model mice, I investigated the potential organ protection by physiological IL6 signaling. Approximately 40% of the CLP mice were below 35°C 24 hours after CLP. Treatment of gp130 for IL6 signaling blockade (gp130 group) increased the rate of moderate hypothermia. When rIL6R was treated (IL6R group), as expected the IL6R group did not show hypothermia. Twenty-four hours after CLP, LD increased more than 4-fold compared to before surgery, but the increase was suppressed to 1.5-fold in the IL6R group. SP-D and MMP-9 in the lung showed the lowest levels in the IL6R group.
From the above, it was suggested that physiological IL6 signaling under sepsis may play a protective role.
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| Academic Significance and Societal Importance of the Research Achievements |
今回の研究結果は、敗血症という急激な侵襲下における生理的なIL6 signalingが体温維持、さらには臓器保護においてかかせないものであることを示唆している。また、生理的なIL6 signalingが不足することにより臓器障害が悪化する可能性も推測された。IL6 signalingは関節リウマチのような慢性的な炎症反応においては遮断することが望ましいが、敗血症のような急激な炎症反応においては、宿主応答の制御の標的として重要な候補になりえることを明らかにできた。
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