Seki, Natsumi

写真a

Affiliation

Faculty of Pharmacy, Department of Pharmacy ( Shiba-Kyoritsu )

Position

Assistant Professor (Non-tenured)/Research Associate (Non-tenured)/Instructor (Non-tenured)
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Licenses and Qualifications 【 Display / hide 】

  • 薬剤師, 2016.05

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Papers 【 Display / hide 】

  • 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 )  2025.12

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

  • 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 )  2023.12

    Research paper (scientific journal), Accepted

    　View Summary

    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)   2023.11

    Research paper (scientific journal), Joint Work, Accepted

  • 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 )  2022.08

    Research paper (scientific journal), Accepted

    　View Summary

    <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 )  2022.07

    Research paper (scientific journal), Lead 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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Reviews, Commentaries, etc. 【 Display / hide 】

  • Adverse effects of methylmercury on gut bacteria and accelerated accumulation of mercury in organs due to disruption of gut microbiota

    Seki N., Akiyama M., Yamakawa H., Hase K., Kumagai Y., Kim Y.G.

    Journal of Toxicological Sciences 46 ( 2 ) 91 - 97 2021

    ISSN  03881350

    　View Summary

    Methylmercury (MeHg), an environmental electrophile, binds covalently to the cysteine residues of proteins in organs, altering protein function and causing cytotoxicity. MeHg has also been shown to alter the composition of gut microbes. The gut microbiota is a complex community, the distur-bance of which has been linked to the development of certain diseases. However, the relationship between MeHg and gut bacteria remains poorly understood. In this study, we showed that MeHg binds covalently to gut bacterial proteins via cysteine residues. We examined the effects of MeHg on the growth of select-ed Lactobacillus species, namely, L. reuteri, L. gasseri, L. casei, and L. acidophilus, that are frequent-ly either positively or negatively correlated with human diseases. The results revealed that MeHg inhibits the growth of Lactobacillus to varying degrees depending on the species. Furthermore, the growth of L. reuteri, which was inhibited by MeHg exposure, was restored by Na<inf>2</inf> S<inf>2</inf> treatment. By comparing mice with and without gut microbiota colonization, we found that gut bacteria contribute to the production of reactive sulfur species such as hydrogen sulfide and hydrogen persulfide in the gut. We also discovered that the removal of gut bacteria accelerated accumulation of mercury in the cerebellum, liver, and lungs of mice subsequent to MeHg exposure. These results accordingly indicate that MeHg is captured and inacti-vated by the hydrogen sulfide and hydrogen persulfide produced by intestinal microbes, thereby providing evidence for the role played by gut microbiota in reducing MeHg toxicity.

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Presentations 【 Display / hide 】

  • 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, 

    2025.12

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

  • 腸内細菌は膵切除後脂肪肝の発症に寄与するか？

    2025.04
    -
    2027.03

    若手研究, Principal investigator

  • 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

    2023.04
    -
    2025.03

    日本学術振興会（JSPS）, 特別研究員奨励費, Other, Principal investigator

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Awards 【 Display / hide 】

  • 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, 2024.07, 日本毒性学会

    Type of Award： Award from Japanese society, conference, symposium, etc.

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Courses Taught 【 Display / hide 】

  • STUDY OF MAJOR FIELD: (CLINICAL PHYSIOLOGY AND THERAPEUTICS)

    2025

  • SEMINAR: (CLINICAL PHYSIOLOGY AND THERAPEUTICS)

    2025

  • RESEARCH FOR BACHELOR'S THESIS 1

    2025

  • PRE-CLINICAL TRAINING FOR HOSPITAL & COMMUNITY PHARMACY

    2025

  • PHARMACEUTICAL-ENGLISH SEMINAR

    2025

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