Elucidation of the mechanism of the innate immune signal that induces hypothalamic inflammation and feeding dysfunction

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08527
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Immunology
• Research Institution: University of Toyama
• Principal Investigator: NAGAI Yoshinori 富山大学, 大学院医学薬学研究部(医学), 客員教授 (30431761)
• Co-Investigator(Renkei-kenkyūsha): WATANABE Yasuharu 富山大学, 大学院医学薬学研究部(医学), 客員准教授 (80646307)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 自然免疫 / 視床下部炎症 / 摂食異常 / レプチン抵抗性

Outline of Final Research Achievements

We found that a TLR signaling molecule TRIF had an important role in the pathogenesis of high-fat diet (HFD)-induced hypothalamic inflammation and leptin resistance. We demonstrated that TRIF was expressed in the hypothalamus of wild-type mice by in situ hybridization. In vivo analyses revealed that HFD- or an intrinsic TLR3 ligand Stathmin-induced inflammation and reduced leptin signaling in the hypothalamus were improved in TRIF-deficent mice compared with wild-type mice. However, TLR3-deficent mice showed different phenotypes from TRIF-deficent mice, suggesting that another molecule other than TLR3 may be responsible for TRIF-induced hypothalamic inflammation and leptin resistance.

Free Research Field

免疫学