Elucidation of the pathophysiology of chronic inflammatory diseases and development of therapies focusing on inflammatory cell death

2021 Fiscal Year Final Research Report

• Project/Area Number: 17K19877
• Research Category: Grant-in-Aid for Challenging Research (Exploratory)
• Allocation Type: Multi-year Fund
• Research Field: Health science and related fields
• Research Institution: Hokkaido University
• Principal Investigator: Asano Mami 北海道大学, 保健科学研究院, 客員研究員 (00779390)
• Co-Investigator(Kenkyū-buntansha): 小澤 岳昌 東京大学, 大学院理学系研究科(理学部), 教授 (40302806) ; 尾崎 倫孝 北海道大学, 保健科学研究院, 教授 (80256510)
• Project Period (FY): 2017-06-30 – 2022-03-31
• Keywords: 細胞死 / 炎症 / 脂肪酸 / 炎症性サイトカイン

Outline of Final Research Achievements

Recent investigations suggest inflammatory cell death release various signals to surrounding cells, and may control biological responses after cell death such as inflammation, immune response, fibrosis, repair, and regeneration.The inflammation cell death have been reported previously in immune cells, such as monocytes and macrophage cells, but rarely in parenchymal cells. We investigated whether various fatty acids were administered to mouse hepatocyte cell lines to produce and secrete inflammatory cytokines, and found that palmitic acid administration induced the production and secretion of inflammatory cytokines and subsequent cell death.

Free Research Field

分子生物学

Academic Significance and Societal Importance of the Research Achievements

この結果は、パルミチン酸が肝傷害を誘導するだけでなく、炎症性サイトカインを積極的に分泌することで肝炎を惹起する可能性、さらには脂肪肝から非アルコール性脂肪肝炎の病態形成・進展へ関与する可能性を示唆している。今後、ステアリン酸などの飽和脂肪酸についても同様の検討を行い、特定の脂肪酸による肝炎発症・促進効果に関して検討する予定である。