Project/Area Number |
26460397
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pathological medical chemistry
|
Research Institution | Toho University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
小島 裕子 順天堂大学, 医学(系)研究科(研究院), 助教 (60231312)
出口 裕 東邦大学, 医学部, 助教 (10287526)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | レポーターマウス / 大腸炎 / IL-11 / 大腸がん / IL-6サイトカインファミリー / 粘膜 / サイトカイン / 修復 / 大腸癌 / il-6サイトカインファミリー / 恒常性 / 腸炎 / 腸管 |
Outline of Final Research Achievements |
Interleukin (IL)-11 is a member of IL-6 family of cytokines that activates signal transducer and activator of transcription 3. Accumulating studies have shown that IL-11 is highly expressed in inflammatory bowl diseases and colorectal cancers in human and mice. However, it remains unclear whether IL-11 plays a crucial role in maintaining tissue homeostasis of the intestine. In this study, using dextran sodium sulfate (DSS)-induced colitis in mice as a model, we found that IL-11 was produced by non-bone marrow-derived cells that were localized in injured intestinal tissues. Moreover, IL-11 primarily acted on intestinal epithelial cells and protected injury of intestinal epithelial cells, thereby attenuating DSS-induced colitis. These findings indicate that IL-11 plays a crucial for maintaining intestinal homeostasis.
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