Duodenal epithelial intercellular junction and IL-33 on the development of dyspepsia

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460939
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Gastroenterology
• Research Institution: Hyogo Medical University
• Principal Investigator: OSHIMA TADAYUKI 兵庫医科大学, 医学部, 講師 (00381814)
• Co-Investigator(Kenkyū-buntansha): FUKUI HIROKAZU 兵庫医科大学, 医学部, 講師 (60378742) ; MIWA HIROTO 兵庫医科大学, 医学部, 教授 (80190833)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 機能性ディスペプシア / タイト結合 / クローディン / 非びらん性胃食道逆流症 / IL-33

Outline of Final Research Achievements

Duodenal epithelial cells expressed claudin (CLDN) 1, CLDN2, CLDN3, CLDN4, CLDN7，CLDN8, CLDN15, CLDN18, JAM-A, Nectin-1, Nectin-3, ZO-1, and ZO-3. The expression of each protein was different in FD patients and CLDN8 seemed to decrease in FD patients.
In vitro, IFNg, but not TNFa or IL-1b, significantly increased IL-33 mRNA compared with untreated cells. The combination of deoxycholic acid (DCA) and IFNg significantly up-regulated IL-33 mRNA compared with IFNg alone, and significantly induced more IL-8 and IL-6 compared with DCA or IFNg alone. DCA and IFNg-induced IL-33 precedes the up-regulation of IL-8 and IL-6. In order to investigate the function of nuclear up-regulated IL-33, the expression was suppressed with siRNA. IL-33 knockdown dampened IFNg-induced IL-8 and IL-6 production. These data suggest that nuclear IL-33 exaggerates the production of inflammatory cytokines.

Free Research Field

消化器内科