| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
It is recognized that macrophages play pivotal roles in the initiation and progression of chronic inflammatory diseases. In response to inflammatory activation via TLR4, macrophages rapidly activate glycolysis, increase inflammatory cytokine expression, acquire M1-like, pro-inflammatory phenotype. By contrast, macrophages increase unsaturated fatty acid synthesis to show M2-like, anti-inflammatory phenotype in the late inflammatory response at 24-48 hour after TLR4 activation. It is likely that unsaturated fatty acids inhibit inflammatory signal, induce anti-inflammatory genes simultaneously by acting as ligands of GPCR and nuclear receptors. These results suggest the functional switch from M1-like to M2-like, and the metabolic switch from glycolysis to lipid metabolism are tightly linked and coordinately regulated during inflammatory response, and these temporal regulatory programs are important for proper inflammatory activation and resolution.
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