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Analyse of Leptin signal in Inflammatory bowel disease

Research Project

Project/Area Number 17K19668
Research Category

Grant-in-Aid for Challenging Research (Exploratory)

Allocation TypeMulti-year Fund
Research Field General internal medicine and related fields
Research InstitutionKeio University

Principal Investigator

Sujino Tomohisa  慶應義塾大学, 医学部(信濃町), 特任講師 (40464862)

Project Period (FY) 2017-06-30 – 2019-03-31
Project Status Completed (Fiscal Year 2018)
Budget Amount *help
¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Keywords炎症性腸疾患 / レプチン / 腸炎 / 肥満 / 腸管免疫細胞
Outline of Final Research Achievements

Leptin is a type of hormone and is known to act on brain, muscle and brown fat cells in the brain after eating, and play a role in insulin sensitivity and suppression of blood sugar elevation. In recent years, it has been discovered that leptin receptors are also present on T cells, and it has been shown that leptin deficiency is less likely to be induced in various enteritis models. The downstream signal of leptin signal is STAT3 pathway, mTOR / Akt pathway, and the former paper has been shown to be essential for Th17 cell induction. We found that the mTOR / AKt signal downstream of leptin is important in the induction of anti-inflammatory CD4CD8aa T cells in the intestinal epithelium.

Academic Significance and Societal Importance of the Research Achievements

レプチンのレセプター下流のSTAT/mTORについて検討した。CD4特異的にSTAT3を上昇させるSOCSfl/fl:CD4creマウスではCD4CD8aaは有意に減少しない。レプチンシグナル下流におけるmTORに着目して腸管上皮内CD4CD8aa細胞の分化誘導との関連性を検討する。mTORシグナルは細胞内代謝とくに解糖系に必要な分子であり、mTORが活性化することでTh17細胞に分化することが知られている。近年細胞の分化増殖に代謝機構が重要視されており、細胞内の代謝調節という切り口から腸管上皮内の細胞の分化誘導機能を解明することで炎症性腸疾患の病態解明、治療方法を確立できる可能性がある、

Report

(3 results)
  • 2018 Annual Research Report   Final Research Report ( PDF )
  • 2017 Research-status Report
  • Research Products

    (4 results)

All 2018 2017

All Journal Article (3 results) (of which Peer Reviewed: 2 results,  Open Access: 2 results) Presentation (1 results) (of which Int'l Joint Research: 1 results)

  • [Journal Article] Toll-Like Receptor 7 Agonist-Induced Dermatitis Causes Severe Dextran Sulfate Sodium Colitis by Altering the Gut Microbiome and Immune Cells.2018

    • Author(s)
      Kiyohara H, Sujino T, Teratani T, Miyamoto K, Arai MM, Nomura E, Harada Y, Aoki R, Koda Y, Mikami Y, Mizuno S, Naganuma M, Hisamatsu T, Kanai T.
    • Journal Title

      Cell Mol Gastroenterol Hepatol.

      Volume: 7 Issue: 1 Pages: 135-156

    • DOI

      10.1016/j.jcmgh.2018.09.010

    • Related Report
      2018 Annual Research Report
    • Peer Reviewed / Open Access
  • [Journal Article] Steroid-refractory extensive enteritis complicated by ulcerative colitis successfully treated with adalimumab2017

    • Author(s)
      Okabayashi Shinji、Kobayashi Taku、Sujino Tomohisa、Ozaki Ryo、Umeda Satoko、Toyonaga Takahiko、Saito Eiko、Nakano Masaru、Tablante Maria Carla、Morinaga Shojiroh、Hibi Toshifumi
    • Journal Title

      intestinal research

      Volume: 15 Issue: 4 Pages: 535-535

    • DOI

      10.5217/ir.2017.15.4.535

    • Related Report
      2017 Research-status Report
    • Peer Reviewed / Open Access
  • [Journal Article] Intestinal immune response is regulated by gut microbe2017

    • Author(s)
      TANEMOTO Shun、SUJINO Tomohisa、KANAI Takanori
    • Journal Title

      Japanese Journal of Clinical Immunology

      Volume: 40 Issue: 6 Pages: 408-415

    • DOI

      10.2177/jsci.40.408

    • NAID

      130006319639

    • ISSN
      0911-4300, 1349-7413
    • Related Report
      2017 Research-status Report
  • [Presentation] intestinal CD4CD8aa cells development in gut2017

    • Author(s)
      Tomohisa Sujino
    • Organizer
      Mucosal Immunology conference
    • Related Report
      2017 Research-status Report
    • Int'l Joint Research

URL: 

Published: 2017-07-21   Modified: 2020-03-30  

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