| Project/Area Number |
15K08470
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Bacteriology (including mycology)
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | サルモネラ / III型エフェクター / NF-κB / 炎症制御 / サルモネラ属細菌 / NF-κB活性化制御 |
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| Outline of Final Research Achievements |
We have identified the signal regulated effectors (Sres) which inhibit TNFα-induced NF-κB activation. In this study, we tried to determine the role of Sres in Salmonella pathogensis. SreA, SreB, and SreC are highly homology to one another and have the consensus zinc metalloprotease HEXXH motif. We showed that SreA, SreB, or SreC directly cleaved NF-κB p65, but the protease activity of SreC is lower than that of SreA or SreB. These results suggest that because of their redundant role in cleaving p65, the effect of SreC could be masked by SreA and SreB. Therefore, SreC may not be necessary to block NF-κB signaling in Salmonella infection. Unfortunately, we found no significant differences in the level of CFU in different tissues and intestinal inflammation in mice orally inoculated with S. Typhimurium wild-type or sreAB, or sreABC mutants.
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