2015 Fiscal Year Final Research Report
Innate immunity-mediated regulation on the induction of precancerous lesions in the stomach.
| Project/Area Number |
25460925
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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 |
Gastroenterology
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| Research Institution | Tohoku University |
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Principal Investigator |
Asano Naoki 東北大学, 大学病院, 助教 (20526454)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | NOD1 / Helicobacter pylori |
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| Outline of Final Research Achievements |
Innate immunity-related molecule NOD1 suppressed Helicobacter pylori (H. pylori) infection induced Cdx2 and Muc2 induction and NF-κB p65 activation in gastric epithelial cells. On the other hand, NOD1 was required for the maintenance of ATP4a expression. The changes in gene expression upon H. pylori infection were observed as induction of intestinal metaplasia and gastric mucosal atrophy in the stomachs of H. pylori-infected NOD1-deficient mice 12 months after infection. The expression of TRAF3 was lower in these mice compared to NOD1-intact mice and this could be one of the causes for the induction of precancerous lesions in H. pylori-infected stomach.
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| Free Research Field |
消化器内科
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