Analyses of the immune cells involving intestinal inflammation and its application for development of foods with intestinal barrier-protecting activity

2015 Fiscal Year Final Research Report

• Project/Area Number: 25292074
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Food science
• Research Institution: Hiroshima University
• Principal Investigator: Soichi TANABE 広島大学, 生物圏科学研究科, 教授 (90272624)
• 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)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: Caco-2 / CD40 / colitis / tight junction / baｃterial metabolite / lactic acid bacteria / bidifobacteria

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.

Free Research Field

食品機能学