Kim, Yungi



Faculty of Pharmacy 創薬研究センター (Shiba-Kyoritsu)


Professor (Non-tenured)

Related Websites

Career 【 Display / hide

  • 2006.01

    University of Michigan, Department of Pathology, Post-doctral fellow

  • 2011.07

    筑波大学, 医学医療系, 助教

  • 2013.06

    University of Michigan, Department of Pathology, Research Investigator

  • 2015.06

    Vedanta Biosciences, Inc., Senior Scientist

  • 2016.08

    慶應義塾大学, 薬学部生化学講座, 准教授

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Academic Degrees 【 Display / hide

  • 博士(薬学), 北里大学, 2005.03

Licenses and Qualifications 【 Display / hide

  • 薬剤師, 2000


Research Keywords 【 Display / hide

  • アレルギー

  • 感染免疫

  • 腸内細菌

  • 自然免疫

Research Themes 【 Display / hide

  • 腸内環境調節と炎症性疾患の制御に関する研究, 



Books 【 Display / hide

  • ヒトマイクロバイオーム Vol.2 ~解析技術の進展とデータ駆動型・ターゲット機能型研究最前線~

    金 倫基,  (株)エヌティーエス, 2020.06

    Scope: 第2節 乳幼児の腸内細菌叢の特性

  • 腸内細菌叢を標的とした医薬品と保健機能食品の開発

    金 倫基, 技術情報協会, 2018.09

    Scope: 腸内細菌叢の創薬応用の研究開発の現状と可能性について

  • ヒトマイクロバイオーム研究最前線

    金 倫基渋谷 彰, (株)エヌ・ティー・エス, 2016.03

    Scope: 腸内細菌叢と喘息

Papers 【 Display / hide

  • Turicibacter and Acidaminococcus predict immune-related adverse events and efficacy of immune checkpoint inhibitor

    Hamada K., Isobe J., Hattori K., Hosonuma M., Baba Y., Murayama M., Narikawa Y., Toyoda H., Funayama E., Tajima K., Shida M., Hirasawa Y., Tsurui T., Ariizumi H., Ishiguro T., Suzuki R., Ohkuma R., Kubota Y., Sambe T., Tsuji M., Wada S., Kiuchi Y., Kobayashi S., Kuramasu A., Horiike A., Kim Y.G., Tsunoda T., Yoshimura K.

    Frontiers in Immunology Accepted 2023.04

    Research paper (scientific journal), Joint Work, Accepted


    Osa S., Enoki Y., Miyajima T., Akiyama M., Fujiwara Y., Taguchi K., Kim Y.G., Matsumoto K.

    Shock (Shock)  59 ( 3 ) 417 - 425 2023.03

    ISSN  10732322

     View Summary

    Background: Patients with underlying skeletal muscle atrophy are likely to develop aggravated sepsis. However, no study has experimentally verified the association between the prognosis of sepsis and muscle atrophy, and the mechanism of aggravation of sepsis under muscle atrophy remains unclear. In this study, we investigated the effect of skeletal muscle atrophy induced by sciatic denervation (DN), an experimental muscle atrophy model, on sepsis prognosis. Methods: Skeletal muscle atrophy was induced by DN of the sciatic nerve in C57BL/6J male mice. Cecal ligation and puncture (CLP) was performed to induce sepsis. Results: The survival rates of the sham and DN groups 7 days after CLP were 63% and 35%, respectively, wherein an approximately 30% reduction was observed in the DN group (P < 0.05, vs. sham-CLP). The DN group had a higher bacterial count in the blood 48 h after CLP (P < 0.05, vs. sham-CLP). Notably, NOx (a metabolite of nitric oxide) concentrations in DN mice were higher than those in sham mice after CLP (P < 0.05, vs. sham-CLP), whereas serum platelet levels were lower 48 h after CLP (P < 0.05, vs. sham-CLP). In organ damage analysis, DN mice presented increased protein expression of the kidney injury molecule (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL), a kidney injury marker, after CLP (NGAL 48 h after CLP, P < 0.05, vs. sham-CLP; KIM-1 24 h after CLP, P < 0.01, vs. sham-CLP). Furthermore, nitro tyrosine levels in the kidneys of DN mice were higher 48 h after CLP compared with those in sham-CLP mice, indicating the accumulation of nitrative stress (P < 0.05, vs. sham-CLP). Serum cytokine levels were increased in both groups after CLP, but decreased in the sham group 48 h after CLP and remained consistently higher in the DN group (tumor necrosis factor [TNF]-α: P < 0.05, sham-CLP vs. DN-CLP; interleukin (IL)-1β: P < 0.01, sham-CLP vs. DN-CLP; IL-6: P < 0.05, DN vs. DN-CLP; IL-10: P < 0.05, sham-CLP vs. DN-CLP). Conclusions: We verified that skeletal muscle atrophy induced by DN is associated with poor prognosis after CLP-induced sepsis. Importantly, mice with skeletal muscle atrophy presented worsening sepsis prognosis at late onset, including prolonged infection, persistent inflammation, and kidney damage accumulation, resulting in delayed recovery.

  • Dietary-protein sources modulate host susceptibility to Clostridioides difficile infection through the gut microbiota

    Yakabe K., Higashi S., Akiyama M., Mori H., Murakami T., Toyoda A., Sugiyama Y., Kishino S., Okano K., Hirayama A., Gotoh A., Li S., Mori T., Katayama T., Ogawa J., Fukuda S., Hase K., Kim Y.G.

    Cell Reports (Cell Press)  Accepted ( 11 )  2022.09

    Research paper (scientific journal), Joint Work, Last author, Corresponding author, Accepted

     View Summary

    Clostridioides difficile causes nosocomial antibiotic-associated diarrhea on a global scale. Susceptibility to C. difficile infection (CDI) is influenced by the composition and metabolism of gut microbiota, which in turn are affected by diet. However, the mechanism underlying the interplay between diet and gut microbiota that modulates susceptibility to CDI remains unclear. Here, we show that a soy protein diet increases the mortality of antibiotic-treated, C. difficile-infected mice while also enhancing the intestinal levels of amino acids (aas) and relative abundance of Lactobacillus genus. Indeed, Ligilactobacillus murinus-mediated fermentation of soy protein results in the generation of aas, thereby promoting C. difficile growth, and the process involves the anchored cell wall proteinase PrtP. Thus, mutual interaction between dietary protein and the gut microbiota is a critical factor affecting host susceptibility to CDI, suggesting that dietary protein sources can be an important determinant in controlling the disease.

  • D-Tryptophan suppresses enteric pathogen and pathobionts and prevents colitis by modulating microbial tryptophan metabolism

    Seki N., Kimizuka T., Gondo M., Yamaguchi G., Sugiura Y., Akiyama M., Yakabe K., Uchiyama J., Higashi S., Haneda T., Suematsu M., Hase K., Kim Y.G.

    iScience (iScience)  25 ( 8 )  2022.08

    Research paper (scientific journal), Corresponding author, Accepted

     View Summary

    D-Amino acids (D-AAs) have various functions in mammals and microbes. D-AAs are produced by gut microbiota and can act as potent bactericidal molecules. Thus, D-AAs regulate the ecological niche of the intestine; however, the actual impacts of D-AAs in the gut remain unknown. In this study, we show that D-Tryptophan (D-Trp) inhibits the growth of enteric pathogen and colitogenic pathobionts. The growth of Citrobacter rodentium in vitro is strongly inhibited by D-Trp treatment. Moreover, D-Trp protects mice from lethal C. rodentium infection via reduction of the pathogen. Additionally, D-Trp prevents the development of experimental colitis by the depletion of specific microbes in the intestine. D-Trp increases the intracellular level of indole acrylic acid (IA), a key molecule that determines the susceptibility of enteric microbes to D-Trp. Treatment with IA improves the survival of mice infected with C. rodentium. Hence, D-Trp could act as a gut environmental modulator that regulates intestinal homeostasis.

  • Cooperative action of gut microbiota-accessible carbohydrates improves host metabolic function

    Tomioka S., Seki N., Sugiura Y., Akiyama M., Uchiyama J., Yamaguchi G., Yakabe K., Ejima R., Hattori K., Kimizuka T., Fujimura Y., Sato H., Gondo M., Ozaki S., Honme Y., Suematsu M., Kimura I., Inohara N., Núñez G., Hase K., Kim Y.G.

    Cell Reports (Cell Press)  40 ( 3 ) 111087 2022.07

    Research paper (scientific journal), Joint Work, Corresponding author, Accepted

     View Summary

    Microbiota-accessible carbohydrates (MACs) exert health-promoting effects, but how each MAC impacts gut microbiota and regulates host physiology remains unclear. Here, we show that L-arabinose and sucrose cooperatively act on gut microbiota and exert anti-obesogenic effects. Specifically, L-arabinose, a monosaccharide that is poorly absorbed in the gut and inhibits intestinal sucrase, suppresses diet-induced obesity in mice in the presence of sucrose. Additionally, the suppressive effect of L-arabinose on adiposity is abrogated in mice lacking the short-chain fatty acid (SCFA) receptors GPR43 and GPR41. Mechanistically, L-arabinose increases the relative abundance of acetate and propionate producers (e.g., Bacteroides), while sucrose enhances SCFA production. Furthermore, L-arabinose and sucrose activate the glycolytic and pentose phosphate pathways of Bacteroides, respectively, indicating that they synergistically promote acetate production through distinct pathways. These findings suggest that each MAC has a unique property and thus may serve as a precision gut-microbiota modulator to promote host homeostasis.

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Papers, etc., Registered in KOARA 【 Display / hide

Reviews, Commentaries, etc. 【 Display / hide

  • マイクロバイオーム創薬の現状と課題

    金 倫基

    Trends of Nutrition 栄養 (株式会社ジェフコーポレーション)  38 ( 1 ) 5 - 9 2023.04

    Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media), Lead author, Corresponding author

  • 腸内細菌による肥満制御と実用化の可能性

    内山 純, 金 倫基

    炎症と免疫 30 ( 6 ) 502 - 506 2022.11

    Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media), Corresponding author

  • 腸内細菌叢に影響を与える食事因子

    山口元輝, 金 倫基

    化学と生物 (国際文献社)  60 ( 4 ) 156 - 160 2022.04

    Joint Work, Last author

  • 腸内細菌叢の変動因子と生活習慣病

    山口 元輝, 秋山 雅博, 金 倫基

    機能性食品と薬理栄養 15 ( 4 ) 212 - 217 2022.02

    Article, review, commentary, editorial, etc. (scientific journal), Joint Work

  • 炎症性腸疾患をターゲットにした腸内細菌製剤の開発と現状

    矢加部 恭輔, 金 倫基

    Medical Science Digest (ニューサイエンス社)  47 ( 11 ) 6 - 10 2021.10

    Article, review, commentary, editorial, etc. (scientific journal), Joint Work

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Presentations 【 Display / hide

  • 腸内環境制御によるサクセスフルエイジングの実現

    金 倫基



    Oral presentation (invited, special), プロダクティブ・エイジング コンソーシアム(PAC)

  • 腸内細菌の創薬応用

    金 倫基

    腸内デザイン学会 腸内環境をデザインする~新たな「腸内細菌叢学」を目指して~, 


    Symposium, workshop panel (nominated)

  • 抗肥満作用を発揮する腸内細菌関連代謝物の探索

    金 倫基

    第20回日本抗加齢医学会総会 腸内細菌の臨床応用 ―便移植からポストバイオティクスまで, 


    Oral presentation (invited, special)

  • 抗肥満作用を発揮する腸内細菌由来代謝物の探索

    金 倫基



    Symposium, workshop panel (nominated)

  • 腸内細菌と肥満

    金 倫基

    第64回日本薬学会関東支部大会 シンポジウムS5 宿主防御機構の新しい視点, 


    Symposium, workshop panel (nominated)

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Research Projects of Competitive Funds, etc. 【 Display / hide

  • 炎症性腸疾患における腸内細菌病因説の検証


    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Challenging Research (Exploratory), Principal investigator

  • Identification of microbiota-associated metabolite which protects against


    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (B), Principal investigator

  • 腸内細菌叢の成熟に伴う腸管病原菌に対する感染抵抗性獲得機構


    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Young Scientists (A), Principal investigator


Courses Taught 【 Display / hide











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