Analysis of A20, modulator of H. pylori associated gastritis.
| Project/Area Number |
24590418
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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 |
Human pathology
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| Research Institution | Oita University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ヘリコバクターピロリ / 胃炎 / 消化器病理 / NF-kB / A20 |
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| Outline of Final Research Achievements |
H. pylori is capable to induce inflammatory responses from host cells through NF-kB. However, little has been known about the process by which gastric epithelial cells counteract H. pylori induced-NF-kB activation to avoid overreactions. A20 is well-known as a NF-kB suppressor and proapoptotic protein. In this study, we investigated the role of A20 in H. pylori-gastric epithelium interaction. We found that upon H. pylori infection, A20 was upregulated in a time- and MOI-dependent manner. A20 mRNA increased sharply within 3 hours and then decreased gradually to the baseline after 36 hours. We transfected cagA vector and H. pylori peptidoglycan into gastric epithelial cells. We found that the transfection of these two agents resulted in a significant increase of A20 expression. These findings indicate that H. pylori induces A20 expression in host cell to restrain H. pylori-activated NF-kB. This negative feed-back loop will establish the balance between host and infectant.
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Report
(4 results)
Research Products
(2 results)
