関 夏実 ( セキ ナツミ )

Seki, Natsumi

写真a

所属(所属キャンパス)

薬学部 薬学科 ( 芝共立 )

職名

助教(有期)

免許・資格 【 表示 / 非表示

  • 薬剤師, 2016年05月

 

論文 【 表示 / 非表示

  • Increased intestinal Lactobacillus abundance in post-pancreatectomysteatotic liver disease is associated with altered bile acid metabolism and FXR–FGF19 pathway suppression

    Kohta Iguchi, Natsumi Seki, Yuki Sugiura, Rae Maeda, Kenzo Nakano, Takayuki Kawai, Yukihiro Okuda, Ryo Kamimura, Yoichiro Uchida, Akihiro Hamasaki, Kojiro Taura, Hiroaki Terajima

    Gut Microbes Reports  3 ( 1 )  2025年12月

    研究論文(学術雑誌), 共著, 筆頭著者, 査読有り

  • Amino acid catabolite markers for early prognostication of pneumonia in patients with COVID-19

    Maeda R., Seki N., Uwamino Y., Wakui M., Nakagama Y., Kido Y., Sasai M., Taira S., Toriu N., Yamamoto M., Matsuura Y., Uchiyama J., Yamaguchi G., Hirakawa M., Kim Y.G., Mishima M., Yanagita M., Suematsu M., Sugiura Y.

    Nature Communications 14 ( 1 )  2023年12月

     概要を見る

    Effective early-stage markers for predicting which patients are at risk of developing SARS-CoV-2 infection have not been fully investigated. Here, we performed comprehensive serum metabolome analysis of a total of 83 patients from two cohorts to determine that the acceleration of amino acid catabolism within 5 days from disease onset correlated with future disease severity. Increased levels of de-aminated amino acid catabolites involved in the de novo nucleotide synthesis pathway were identified as early prognostic markers that correlated with the initial viral load. We further employed mice models of SARS-CoV2-MA10 and influenza infection to demonstrate that such de-amination of amino acids and de novo synthesis of nucleotides were associated with the abnormal proliferation of airway and vascular tissue cells in the lungs during the early stages of infection. Consequently, it can be concluded that lung parenchymal tissue remodeling in the early stages of respiratory viral infections induces systemic metabolic remodeling and that the associated key amino acid catabolites are valid predictors for excessive inflammatory response in later disease stages.

  • Hydrogen gas and the gut microbiota are potential biomarkers for the development of experimental colitis in mice

    Yuta Fujiki, Takahisa Tanaka, Kyosuke Yakabe, Natsumi Seki, Masahiro Akiyama, Ken Uchida, Yun-Gi Kim

    Gut Microbiome (Camb)  2023年11月

    共著

  • 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 25 ( 8 )  2022年08月

     概要を見る

    <inf>D</inf>-Amino acids (<inf>D</inf>-AAs) have various functions in mammals and microbes. <inf>D</inf>-AAs are produced by gut microbiota and can act as potent bactericidal molecules. Thus, <inf>D</inf>-AAs regulate the ecological niche of the intestine; however, the actual impacts of <inf>D</inf>-AAs in the gut remain unknown. In this study, we show that <inf>D</inf>-Tryptophan (<inf>D</inf>-Trp) inhibits the growth of enteric pathogen and colitogenic pathobionts. The growth of Citrobacter rodentium in vitro is strongly inhibited by <inf>D</inf>-Trp treatment. Moreover, <inf>D</inf>-Trp protects mice from lethal C. rodentium infection via reduction of the pathogen. Additionally, <inf>D</inf>-Trp prevents the development of experimental colitis by the depletion of specific microbes in the intestine. <inf>D</inf>-Trp increases the intracellular level of indole acrylic acid (IA), a key molecule that determines the susceptibility of enteric microbes to <inf>D</inf>-Trp. Treatment with IA improves the survival of mice infected with C. rodentium. Hence, <inf>D</inf>-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 40 ( 3 )  2022年07月

     概要を見る

    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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研究発表 【 表示 / 非表示

  • Komaroviquinone-Derived Compounds Induce Immunogenic Cell Death and Suppress Tumor Growth in vivo

    Natsumi Seki, Keita Yoshikawa, Taisei Fujinami, Koki Kurita, Himari Yamada, Yusuke Yamamoto, Yutaka Suto, Maiko Matsushita

    第54回日本免疫学会学術集会, 

    2025年12月

競争的研究費の研究課題 【 表示 / 非表示

  • 腸内細菌は膵切除後脂肪肝の発症に寄与するか?

    2025年04月
    -
    2027年03月

    関 夏実, 若手研究, 補助金,  研究代表者

  • 腸内細菌叢由来の代謝物は、どのように宿主脳機能に影響を与えるか

    2023年04月
    -
    2025年03月

    日本学術振興会(JSPS), 特別研究員奨励費, その他,  研究代表者

受賞 【 表示 / 非表示

  • 第14回 2024年度 ファイザー賞

    Natsumi Seki, Masahiro Akiyama, Hiroto Yamakawa, Koji Hase, Yoshito Kumagai, Yun-Gi Kim, 2024年07月, 日本毒性学会

    受賞区分: 国内学会・会議・シンポジウム等の賞

 

担当授業科目 【 表示 / 非表示

  • 課題研究(病態生理学)

    2025年度

  • 演習(病態生理学)

    2025年度

  • 卒業研究1(薬学科)

    2025年度

  • 実務実習事前学習(実習)

    2025年度

  • 英語演習(薬学科)

    2025年度

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