Dysregulation of immune system and metabolic system that leads to the chronic inflammation in macrophage

2016 Fiscal Year Final Research Report

• Project/Area Number: 26461142
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Cardiovascular medicine
• Research Institution: Tokyo Medical and Dental University
• Principal Investigator: OISHI YUMIKO 東京医科歯科大学, 難治疾患研究所, テニュアトラック准教授 (80435734)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: マクロファージ

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.

Free Research Field

循環器内科学