Carbon monoxide releasing molecule attenuate pulmonary injury through modulating macrophage M1/M2 phenotype
Project/Area Number |
25861247
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Respiratory surgery
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Research Institution | Osaka City University |
Principal Investigator |
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Research Collaborator |
Nishiyama Noritoshi 大阪市立大学, 大学院医学研究科, 准教授 (90438226)
Yamamoto-Oka hiroko 大阪市立大学, 大学院医学研究科, 大学院生
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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Keywords | 肺保護 / 一酸化炭素 / マクロファージ / 敗血症 / 肺障害 / 好中球 / 急性炎症 / 臓器保護効果 / 細胞特異的 / M1/M2 |
Outline of Final Research Achievements |
The aim of this project was to assess the difference modulation of septic lung injury by water-soluble carbon monoxide releasing molecule-3 (CORM-3) via several administrations (intra-venous, peritoneal, and tracheal) in septic mouse model (in vivo). CORM-3 administrated by intra-venous and peritoneal were attenuated lung injury, although those by intra-tracheal was not attenuated lung injury. Next, modulation of M1/M2 phenotype in alveolar macrophages (AMs) by CORM-3 was assessed in vitro. Treatment of unstimulated AMs with CORM-3 promoted progression of M2 phenotype (the increased expression of CD206 and Ym-1). CORM-3 reduced LPS/IFNγ (M1 stimulus)-induced expression of iNOS protein. On the contrary, CORM-3 acutely upregulated CD206 and Ym-1 levels in IL-4/IL-13 (M2 stimulus)-treated AMs. CORM-3 can modulate macrophage M1/M2-phenotype in vitro via continuous suppression of iNOS expression in M1-polarized AMs and upregulation of CD206 and Ym-1 proteins in M2-polarized AMs.
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Report
(4 results)
Research Products
(2 results)