Functional analysis of the Salmonella type III effectors that regulate the host's immune response using the streptomycin mouse model

2015 Fiscal Year Final Research Report

• Project/Area Number: 25293106
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Bacteriology (including mycology)
• Research Institution: Kitasato University
• Principal Investigator: Okada Nobuhiko 北里大学, 薬学部, 教授 (80194364)
• Co-Investigator(Kenkyū-buntansha): HANEDA TAKESHI 北里大学, 薬学部, 講師 (00348591) ; MORIYA CHIKAYA 北里大学, 薬学部, 助教 (90518101)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: サルモネラ / サルモネラ腸炎 / Ⅲ型エフェクター / NF-κB / Ⅲ型分泌機構

Outline of Final Research Achievements

Microbial infections usually lead to host innate immune responses and inflammation. The enteropathogenic bacteria Salmonella Typhimurium utilizes a type III secretion system to induce intestinal inflammation by delivering specific effector proteins that stimulate signal transduction pathways resulting in the production of pro-inflammatory cytokines. In this study, we have identified Salmonella effector proteins that inhibit the NF-κB signaling pathway. A family of SseK proteins is bound to TRADD and FADD. Also, we show that these effector proteins SreA and SreB are metalloproteases that cleave the RelA transcription factor. These results indicate that Salmonella can evolve determinants to regulate host inflammatory response and that those determinants can contribute to the development of Salmonella infection.

Free Research Field

医歯薬学