2023 Fiscal Year Final Research Report
Role of chemokine MIP1-gamma in the pathogenesis of inflammatory bowel disease and hepatitis
Project/Area Number |
22K20860
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Research Category |
Grant-in-Aid for Research Activity Start-up
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Allocation Type | Multi-year Fund |
Review Section |
0902:General internal medicine and related fields
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Research Institution | Oita University |
Principal Investigator |
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Project Period (FY) |
2022-08-31 – 2024-03-31
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Keywords | 炎症性腸疾患 / 自己免疫性肝炎 / ケモカイン / MIP1-γ |
Outline of Final Research Achievements |
The aim of this study is to clarify the role of the chemokine MIP1-γ in the pathogenesis of two intractable diseases in the field of gastroenterology, inflammatory bowel disease and autoimmune hepatitis, using mouse disease models. MIP1-γdeficient mice showed severe intestinal inflammation in response to DSS, which is commonly used in studies for IBDs, suggesting an involvement of MIP1-γin immune regulation. In Con A hepatitis, which was used as a model of autoimmune hepatitis, there was a trend toward greater survival in MIP1-γ-deficient mice. However, due to an experimental error, it is difficult to evaluate the precise role of MIP1-γ in autoimmune hepatitis. An alternative hepatitis model is required.
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Free Research Field |
消化器分野
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Academic Significance and Societal Importance of the Research Achievements |
炎症性腸疾患、自己免疫性肝炎は未だ原因不明の消化器疾患であり、様々な分子標的薬による治療が行われているが、治療抵抗性の症例も相当数存在する。本研究は、これらの難病の原因解明および新薬開発の一助となる可能性がある。今回、実験的大腸炎モデルにおいて、MIP1-γ遺伝子欠損マウスが野生型マウスと比較して増悪する傾向が示された。そのため、今後マウスモデルを用いて増悪化の機序を解明し、臨床応用に向けた研究に繋げていきたい。
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