New activation pathway for inflammasome

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H04730
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Bacteriology (including mycology)
• Research Institution: Tokyo Medical and Dental University
• Principal Investigator: SUZUKI Toshihiko 東京医科歯科大学, 大学院医歯学総合研究科, 教授 (10292848)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: インフラマゾーム / 慢性炎症 / カスパーゼ-1

Outline of Final Research Achievements

Inflammasome is macromolecule complexes in the host cells upon being activated by pathogen infection or metabolites in the body. Caspase-1 activation is finely regulated by inflammasome that forms with Nod-like receptors (NLRs), and then activated caspase-1 can cleave pro-IL-1 or IL-18, and convert their bioactive cytokines. Among NLRs, NLRP3 is involved in chronic inflammatory diseases such as type II Diabetes or gout, because NLRP3 inflammasome can be activated by several metabolites including saturated fatty acids, cholesterol or uric acids crystals. In this work, we found new signaling pathway for activating NLRP3 inflammasome. The lysosome integrity-galectin-3 accumulation-NLRP3 activation axis may provide important insights into NLRP3 inflammasome activation in host cells.

Free Research Field

細菌学、免疫学