| 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)
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| 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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