Elucidation of fibrosis mechanism in inflammatory bowel disease and its application to molecular targeting therapy

2016 Fiscal Year Final Research Report

• Project/Area Number: 26460976
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Gastroenterology
• Research Institution: Yokohama City University
• Principal Investigator: SHIBATA Wataru 横浜市立大学, 先端医科学研究センター, 准教授 (00435819)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 線維化 / NF-kB

Outline of Final Research Achievements

Here we investigated the role of numerous fibroblasts in the inflamed region on fibrosis, focusing on the activation of the expected NF-κB pathway, which is particularly relevant. NF-κB deficient mice specific for myofibroblasts considered to be involved in fibrosis were prepared, and dextran sodium sulfate (DSS) intestinal inflammation model and intestinal allograft model were examined. In vitro studies, we used fetal embryonic fibroblast cells. As a result, the number of myofibroblast cells induced by inflammation was less in knockout mice in intestinal inflammation model. αSMA and TGFβ were attenuated in knockout mice in transplanted intestinal tract. In the examination with MEF, expression of TGFβ and inflammatory cytokine by inflammatory stimulation was decreased in knockout MEF, suggesting that the NF-kB pathway was involved in fibrosis formation.

Free Research Field

消化器内科学