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Unveiling the impact of disrupted intracellular iron regulation in intestinal macrophages on the pathophysiology of inflammatory bowel disease

Research Project

Project/Area Number 16K19365
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Gastroenterology
Research InstitutionKitasato University

Principal Investigator

Toyonaga Takahiko  北里大学, 北里研究所病院, 医員 (30773634)

Project Period (FY) 2016-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Keywords鉄 / マクロファージ / 炎症性腸疾患
Outline of Final Research Achievements

The aim of this study was elucidating the intracellular iron dynamics in intestinal macrophages under inflammatory conditions and unveiling the contribution of disrupted iron regulatory mechanism in intestinal macrophages to the pathophysiology of IBD. Using DSS induced acute colitis mouse model, we demonstrated intestinal inflammation increased the expression of ferritin in intestinal macrophages which was followed by the increased expression of ferroportin-1, an iron exporter. In the in vitro experiments using bone marrow-derived murine macrophages, we found decreased IL-12p40 production in Ferroportin1 knock down macrophages compared to the controls after stimulation with LPS. Suppressing ferroportin1 might affect the expression of Nrf2, a transcriptional factor which regulates ferroportin-1 expression and was recently reported to directly suppress the production of proinflammatory cytokines in macrophages and result in the decreased Il12b expression.

Report

(3 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report

URL: 

Published: 2016-04-21   Modified: 2019-03-29  

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