Mechanism of Fas-mediated inflammatory response against bacterial infection in vivo

Research Project

Project/Area Number	26460539
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Bacteriology (including mycology)
Research Institution	Hyogo Medical University
Principal Investigator	Uchiyama Ryosuke 兵庫医科大学, 医学部, 講師 (20456891)
Co-Investigator(Renkei-kenkyūsha)	TSUTSUI Hiroko 兵庫医科大学, 医学部, 主任教授 (40236914) YONEHARA Shin 京都大学, 大学院・生命科学研究科, 教授 (00124503)
Project Period (FY)	2014-04-01 – 2017-03-31
Project Status	Completed (Fiscal Year 2016)
Budget Amount *help	¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000) Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000) Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000) Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Keywords	Fasシグナル / 炎症性サイトカイン / 細菌感染 / Th17/Th1細胞 / 自然免疫 / Fas / IL-17 / IL-1b / Th17 / Listeria
Outline of Final Research Achievements	Fas signaling pathway is known to play a pivotal role in apoptosis induction. In addition, we have revealed that macrophages produced IL-1b by Fas-mediated inflammation in bacterial infection. However, the precise role of Fas-mediated cytokine production in actual pathogen infection was unclear. In this study, we found that Fas-mediated IL-1b contributes to the induction of novel helper T cells which produce IFN-g/IL-17 (called Th17/Th1 cells). This study provides a deeper understanding of the molecular mechanisms of Th17/Th1 induction during pathogenic microbe infection in vivo.