Functional analysis of the Salmonella type III effectors that regulate the host's immune response using the streptomycin mouse model
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 |
|
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
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥17,290,000 (Direct Cost: ¥13,300,000、Indirect Cost: ¥3,990,000)
Fiscal Year 2015: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2014: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2013: ¥7,410,000 (Direct Cost: ¥5,700,000、Indirect Cost: ¥1,710,000)
|
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 / サルモネラ感染症 / 炎症抑制 / マウス腸炎モデル / 腸管感染モデル / 腸炎 / 三型分泌機構 / 三型エフェクター / III型分泌機構 / III型エフェクター |
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.
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Report
(4 results)
Research Products
(23 results)