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KAKEN_17KT0055seika.pdf
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Download
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:221.9 KB
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:Mar 5, 2021 |
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Total downloads since Mar 5, 2021 : 486
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多変量解析による慢性炎症スパイラル形成機構の解明
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タヘンリョウ カイセキ ニ ヨル マンセイ エンショウ スパイラル ケイセイ キコウ ノ カイメイ
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Tahenryō kaiseki ni yoru mansei enshō supairaru keisei kikō no kaimei
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Elucidation of pathogenic mechanism of chronic inflammation
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長谷, 耕二
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ハセ, コウジ
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Hase, Kōji
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慶應義塾大学・薬学部 (芝共立) ・教授
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Research team head
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科研費研究者番号 : 20359714
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2020
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科学研究費補助金研究成果報告書
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2019
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腸内細菌は難消化性多糖類の発酵代謝により短鎖脂肪酸を産生する。短鎖脂肪酸は多様な生理活性を有し、特に酪酸は腸管免疫恒常性維持における鍵因子とみなされている。本研究では我が国で年々増加している潰瘍性大腸炎 (UC) およびクローン病 (CD) 患者における酪酸低下の原因を解析した。CD患者では主要な酪酸産生菌の顕著な減少がクローン病における酪酸産生低下の原因と考えられた。一方で、UC患者では腸内細菌によるムチン糖鎖利用の低下が酪酸産生低下の原因と考えられた。
The dysbiosis of gut microbiota has been implicated in the pathogenesis of inflammatory bowel diseases; however, the underlying mechanisms have not yet been elucidated. Levels of n-butyrate were significantly lower in stools of both CD and UC patients than in stools of healthy subjects. The major n-butyrate producer was particularly underrepresented in CD patients, but not in UC patients. The decrease in butyrate production in UC patients was attributed to abnormal mucin utilisation that is one of the pathways for n-butyrate production.
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研究種目 : 基盤研究 (B) (特設分野研究)
研究期間 : 2017～2019
課題番号 : 17KT0055
研究分野 : 免疫学
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