2015 Fiscal Year Final Research Report
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 |
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| Research Field |
Respiratory surgery
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| Research Institution | Osaka City University |
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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
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | 肺保護 / 一酸化炭素 / マクロファージ |
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| 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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| Free Research Field |
呼吸器外科
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