| Project/Area Number |
25292074
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Food science
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| Research Institution | Hiroshima University |
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Principal Investigator |
Soichi TANABE 広島大学, 生物圏科学研究科, 教授 (90272624)
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| Co-Investigator(Kenkyū-buntansha) |
KAWAMOTO Seiji 広島大学, 大学院先端物質科学研究科, 教授 (90294537)
KIMURA Ikuo 東京農工大学, 大学院農学研究院, 准教授 (80433689)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2015: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥9,490,000 (Direct Cost: ¥7,300,000、Indirect Cost: ¥2,190,000)
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| Keywords | Caco-2 / CD40 / colitis / tight junction / baｃterial metabolite / lactic acid bacteria / bidifobacteria / intestinal barrier / commensal bacteria / bacterial metabolite / HYA / Th17 / bifidobacteria / hypoxia |
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| Outline of Final Research Achievements |
In this study, the effects of gut microbial metabolites on tumor necrosis factor (TNF)-α-induced barrier impairment in Caco-2 cells and dextran sulfate sodium-induced colitis in mice were evaluated. 10-Hydroxy-cis-12-octadecenoic acid (HYA), a gut microbial metabolite of linoleic acid, suppressed TNF-α and dextran sulfate sodium-induced changes in the expression of tight junction-related molecules. HYA also suppressed the expression of TNF receptor 2 (TNFR2) in Caco-2 cells and colonic tissue. Furthermore, HYA significantly up-regulated G protein-coupled receptor (GPR) 40 expression in Caco-2 cells. The barrier-recovering effects of HYA were abrogated by a GPR40 antagonist. Conversely, 10-hydroxyoctadacanoic acid, which is a gut microbial metabolite of oleic acid and lacks Δ12 carbon-carbon double bond, did not show these tight junction-restoring activities and down-regulated GPR40 expression. Therefore, HYA modulates TNFR2 expression, at least in part, by GPR40 pathway.
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