慶應義塾研究者情報データベース

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• 2010年04月

  -

  2012年03月

  総合病院国保旭中央病院, 初期臨床研修医

• 2012年04月

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  2013年03月

  慶應義塾大学医学部, 内科学教室

• 2013年04月

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  2014年03月

  国立病院機構東京医療センター, 内科レジデント

• 2014年04月

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  2018年03月

  慶應義塾大学医学部内科学教室(呼吸器)

• 2016年04月

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  2018年03月

  日本学術振興会, 特別研究員(DC2)

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• 2004年04月

  -

  2010年03月

  慶應義塾大学, 医学部

研究分野 【 表示 ／ 非表示 】

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• ライフサイエンス / 呼吸器内科学

• ライフサイエンス / 感染症内科学

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• 呼吸器感染症

• 気管支拡張症

• 非結核性抗酸菌症

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• 症例で学ぶ肺非結核性抗酸菌症

  長谷川, 直樹, 朝倉, 崇徳, 非結核性抗酸菌症・気管支拡張症研究コンソーシアム, 医学書院, 2020年11月,  ページ数： x, 251p

  • CiNii Research

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• Direct reprogramming of mouse fibroblasts into self-renewable alveolar epithelial-like cells

  Morita A., Ishii M., Asakura T., Yotsukura M., Hegab A.E., Kusumoto T., Namkoong H., Ogawa T., Nakatake Y., Oda M., Saito F., Kamata H., Hamamoto J., Okamori S., Ebisudani T., Yasuda H., Sugimoto S., Kuze Y., Seki M., Suzuki Y., Hasegawa N., Asamura H., Watanabe H., Ko M., Sato T., Ieda M., Fukunaga K.

  Npj Regenerative Medicine 10 （ 1 ） 30 - 30 2025年12月

  　概要を見る

  Direct reprogramming is a breakthrough technology that can alter the fate of cells without the passage of stem cells. However, direct reprogramming of somatic cells into pulmonary alveolar epithelial cells has not yet been achieved. Here, we report the direct reprogramming of mouse tail tips and embryonic fibroblasts into induced pulmonary alveolar epithelial-like cells (iPULs) using four transcription factor-coding genes (Nkx2-1, Foxa1, Foxa2, and Gata6) and three-dimensional culture. The iPULs showed lamellar body-like structures and displayed key properties of pulmonary alveolar epithelial cells. Although the potential for iPULs to morphologically differentiate into alveolar epithelial type 1 cells was limited in vitro, the intratracheal administration of iPULs in a bleomycin-induced mouse model of pulmonary fibrosis led to their integration into the alveolar surface, where they formed both alveolar epithelial type 1 and type 2-like cells. Thus, reprogrammed fibroblasts may represent a new source of pulmonary alveolar epithelial cells for regenerative medicine.

  • Access to Document (DOI)

• Predicting coronavirus disease 2019 severity using explainable artificial intelligence techniques

  Ozawa T., Chubachi S., Namkoong H., Nemoto S., Ikegami R., Asakura T., Tanaka H., Lee H., Fukushima T., Azekawa S., Otake S., Nakagawara K., Watase M., Masaki K., Kamata H., Harada N., Ueda T., Ueda S., Ishiguro T., Arimura K., Saito F., Yoshiyama T., Nakano Y., Muto Y., Suzuki Y., Edahiro R., Murakami K., Sato Y., Okada Y., Koike R., Ishii M., Hasegawa N., Kitagawa Y., Tokunaga K., Kimura A., Miyano S., Ogawa S., Kanai T., Fukunaga K., Imoto S.

  Scientific Reports （Springer Science and Business Media LLC）  15 （ 1 ） 9459 - 9459 2025年12月

  　概要を見る

  Predictive models for determining coronavirus disease 2019 (COVID-19) severity have been established; however, the complexity of the interactions among factors limits the use of conventional statistical methods. This study aimed to establish a simple and accurate predictive model for COVID-19 severity using an explainable machine learning approach. A total of 3,301 patients ≥ 18 years diagnosed with COVID-19 between February 2020 and October 2022 were included. The discovery cohort comprised patients whose disease onset fell before October 1, 2020 (N = 1,023), and the validation cohort comprised the remaining patients (N = 2,278). Pointwise linear and logistic regression models were used to extract 41 features. Reinforcement learning was used to generate a simple model with high predictive accuracy. The primary evaluation was the area under the receiver operating characteristic curve (AUC). The predictive model achieved an AUC of ≥ 0.905 using four features: serum albumin levels, lactate dehydrogenase levels, age, and neutrophil count. The highest AUC value was 0.906 (sensitivity, 0.842; specificity, 0.811) in the discovery cohort and 0.861 (sensitivity, 0.804; specificity, 0.675) in the validation cohort. Simple and well-structured predictive models were established, which may aid in patient management and the selection of therapeutic interventions.

  • Access to Document (DOI)

• Impact of long COVID on the health-related quality of life of Japanese patients: A prospective nationwide cohort study

  Yagi K., Kondo M., Terai H., Asakura T., Kimura R., Takemura R., Tanaka H., Ohgino K., Masaki K., Namkoong H., Chubachi S., Miyata J., Kawada I., Kaido T., Mashimo S., Kobayashi K., Hirano T., Lee H., Sugihara K., Omori N., Watase M., Mochimaru T., Satomi R., Makino Y., Inoue T., Sayama K., Oyamada Y., Ishii M., Sato Y., Fukunaga K.

  Respiratory Investigation 63 （ 4 ） 610 - 616 2025年07月

  ISSN  22125345

  　概要を見る

  Background: Various prolonged systemic symptoms, forming the long coronavirus disease (COVID), have been observed in patients who have recovered from the acute phase of COVID-19. Although previous studies have reported that COVID-19 impacts health-related quality of life (HRQoL), the associations of long COVID symptoms and clinical characteristics with HRQoL remain unclear. This study aimed to clarify these associations using nationwide Japanese epidemiological data. Methods: A prospective nationwide cohort study was conducted on patients with COVID-19 between January 2020 and February 2021 at 26 participating medical institutions in Japan. Various long COVID symptoms and HRQoL scores at 3, 6, and 12 months following diagnosis were collected from 986 participants. Generalized estimating equations (GEE) were used to explore the association between HRQoL scores evaluated using the short form-8 (SF-8), long COVID symptoms, and baseline clinical characteristics. Results: Patients who had one long COVID symptom showed a significantly lower physical component summary score (PCS) and mental component summary score (MCS) compared with those without any symptoms at all time points after diagnosis. GEE revealed that long COVID symptoms, including dyspnea, fatigue, headache, and muscle weakness, were significantly associated with worse PCS, whereas poor concentration, sleep disorders, fatigue, and headache were significantly associated with worse MCS. Severity-related baseline parameters for patients with COVID-19 were significantly associated with worse PCS scores, although these factors were not significantly associated with worse MCS scores. Conclusions: Long COVID symptoms were associated with lower physical and mental HRQoL. Severe outcomes of COVID-19 impacted PCS but not MCS.

  • Access to Document (DOI)

• Sectm1a Depletion Promotes Neutrophil Recruitment during Pneumococcal Pneumonia

  Tanaka H., Kamata H., Ishii M., Asakura T., Namkoong H., Nakagawara K., Morita A., Kusumoto T., Azekawa S., Kaji M., Nagao G., Fukunaga N., Nishimura T., Asakura K., Hasegawa N., Fukunaga K.

  American Journal of Respiratory Cell and Molecular Biology 73 （ 1 ） 60 - 72 2025年07月

  ISSN  10441549

  　概要を見る

  Airway epithelial cells (AECs) play an essential role in the immune response during bacterial pneumonia. Secreted and transmembrane 1a (Sectm1a) is specifically expressed in AECs during early Streptococcus pneumoniae (SP) infection. However, its function remains largely unexplored. Here, we aimed to clarify the function of Sectm1a during serotype 3 pneumococcal pneumonia primarily using an in vivo mouse model. Our findings showed that Type I IFNs directly induced Sectm1a expression in AECs. Sectm1a depletion in an in vivo mouse model improved survival rate and enhanced the clearance of intrapulmonary bacterial burden at an early stage of SP infection. Correspondingly, Sectm1a depletion increased the count of intrapulmonary γδT cells, promoted IL-17A production by these cells, and enhanced intrapulmonary neutrophil responses against SP. Notably, IL-17A production in isolated lung γδT cells was directly suppressed by Sectm1a ex vivo. Furthermore, Sectm1a depletion altered the migration and activation markers of γδT cellsin vivo, indicating that the AEC-derived Sectm1a is associated with the phenotypes of γδT cells. These findings suggest that Type I IFNs may play an important role through AEC-derived Sectm1a in this model, and Sectm1a signaling modulates excessive neutrophil inflammation and influences bacterial clearance by directly altering γδT cell functions during pneumococcal pneumonia. In summary, this study demonstrates that the Type I IFN–Sectm1a pathway could be a potential target to modify the acute response to bacterial pneumonia.

  • Access to Document (DOI)

• STAT3-dependent Regulation of CFTR and Ciliogenesis Is Essential for Mucociliary Clearance and Innate Airway Defense in Hyper-IgE Syndrome.

  Ling Sun, Samantha A Walls, Hong Dang, Nancy L Quinney, Patrick R Sears, Taraneh Sadritabrizi, Koichi Hasegawa, Kenichi Okuda, Takanori Asakura, Xiuya Chang, Meiqi Zheng, Yu Mikami, Felicia U Dizmond, Daniela Danilova, Lynn Zhou, Anshulika Deshmukh, Deborah M Cholon, Giorgia Radicioni, Troy D Rogers, William J Kissner, Matthew R Markovetz, Tara N Guhr Lee, Mark I Gutay, Charles R Esther Jr, Michael Chua, Barbara R Grubb, Camille Ehre, Mehmet Kesimer, David B Hill, Lawrence E Ostrowski, Brian Button, Martina Gentzsch, Chevalia Robinson, Kenneth N Olivier, Alexandra F Freeman, Scott H Randell, Eszter Vladar, Wanda K O'Neal, Richard C Boucher Jr, Gang Chen

  American journal of respiratory and critical care medicine 2025年05月

  　概要を見る

  RATIONALE: Hyper IgE syndrome (STAT3-HIES), also known as Job's syndrome, is a rare immunodeficiency disease typically caused by dominant-negative STAT3 mutations. STAT3-HIES is characterized by chronic pulmonary infection and inflammation, suggesting impaired innate host defense. OBJECTIVES: To identify airway epithelial host defense defects caused by STAT3 mutations that, together with immune dysfunction, contribute to recurrent pulmonary infections in STAT3-HIES. METHODS: STAT3-HIES sputum was analyzed for biochemical and biophysical properties. STAT3-HIES excised lungs were harvested for histology; and bronchial brush samples were collected for RNA sequencing and in vitro culture. A STAT3-HIES-specific R382W mutation, expressed via lentivirus, and STAT3 knockout (CRISPR/Cas9), were studied in normal human bronchial epithelial cells under basal or inflammatory (IL1β)-stimulated conditions. Effects of STAT3 deficiency on transcriptomics, epithelial ion channel, secretory, antimicrobial, and ciliary functions were assessed. MEASUREMENTS AND MAIN RESULTS: STAT3-HIES sputum showed increased mucus concentration and viscoelasticity. STAT3-HIES excised lungs exhibited mucus obstruction and elevated IL1β expression. STAT3 mutations reduced CFTR mRNA and protein levels, impaired CFTR-dependent fluid and mucin secretion, suppressed antimicrobial peptide, cytokine, and chemokine expression, and acidified airway surface liquid at baseline and post-IL1β exposure. Notably, mutant STAT3 suppressed IL1R1 expression. Furthermore, STAT3 mutations impaired multiciliogenesis by blocking commitment to ciliated cell lineages through inhibition of HES6, leading to defective mucociliary transport. Administration of a γ-secretase inhibitor restored HES6 expression, improved ciliogenesis in STAT3 R382W mutant cells. CONCLUSIONS: STAT3 dysfunction leads to multi-component defects in airway epithelial innate defense, which, in conjunction with immune deficiency, contributes to chronic pulmonary infection in STAT3-HIES.

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• ムチン異常集積に着目した肺非結核性抗酸菌症の病態解明

  朝倉, 崇徳

  科学研究費補助金研究成果報告書 2023年

総説・解説等 【 表示 ／ 非表示 】

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• Corrigendum to “Efficacy and safety of long-term macrolide therapy for non-cystic fibrosis bronchiectasis: A systematic review and meta-analysis” [Respir Invest Volume 62 (2024) 1079-1087, (S2212534524001436), (10.1016/j.resinv.2024.09.004)]

  Nakagawa N., Ito M., Asakura T., Horita N., Obase Y., Mukae H.

  Respiratory Investigation 63 （ 2 ） 224 - 225 2025年03月

  ISSN  22125345

  　概要を見る

  The authors regret that the Figure 3 Fig. is incorrect. The correct Fig. is available below. Additionally, the correct sentence on page 1082, lines 1–3, should read: "and reduced sputum volume (grams) (mean difference = −8.24, 95% CI = −14.04 to −2.44, P < 0.01) (Fig. 3c)."[Figure presented] The authors would like to apologise for any inconvenience caused.

  • Access to Document (DOI)

• Corrigendum to ‘Impact of accumulative smoking exposure and chronic obstructive pulmonary disease on COVID-19 outcomes: report based on findings from the Japan COVID-19 task force’ [IJID 128 (2023) 121–127, (S1201971222006555), (10.1016/j.ijid.2022.12.019)]

  Watase M., Masaki K., Chubachi S., Namkoong H., Tanaka H., Lee H., Fukushima T., Otake S., Nakagawara K., Kusumoto T., Asakura T., Kamata H., Ishii M., Hasegawa N., Oyamada Y., Harada N., Ueda T., Ueda S., Ishiguro T., Arimura K., Saito F., Yoshiyama T., Nakano Y., Mutoh Y., Suzuki Y., Edahiro R., Sano H., Sato Y., Okada Y., Koike R., Kitagawa Y., Tokunaga K., Kimura A., Imoto S., Miyano S., Ogawa S., Kanai T., Fukunaga K.

  International Journal of Infectious Diseases 151 2025年02月

  ISSN  12019712

  　概要を見る

  The authors would like to point out that the caption for Figure 2 in the published version of their paper contained an error. The correct caption is below: Figure 2 legend (corrected version): (a) Incidence of IMV among non-COPD patients classified by PY and COPD patients. (b) Results of the univariate analysis of need for IMV on all smoker patients (b-1), smoker patients aged 65 years or younger (b-2), and smoker patients over 65 years old (b-3). **p< 0.001, *p<0.05. IMV, invasive mechanical ventilation; COPD, chronic obstructive pulmonary disease; PY, pack-year.

  • Access to Document (DOI)

• 慢性閉塞性肺疾患(COPD)における腸内細菌叢・代謝産物の役割

  大竹史朗, 中鉢正太郎, 宮本潤基, 島田嵩, 朝倉崇徳, 宮田純, 加畑宏樹, 入江潤一郎, 福永興壱

  日本内科学会雑誌 114 2025年

  ISSN  0021-5384

• 【気管支拡張症-温故知新 注目され始めた一大カテゴリー】気管支拡張症の病態とその解明に向けて 気管支拡張症の臨床像と病態 重症度,増悪とそのメカニズム,バイオマーカーの可能性

  朝倉 崇徳

  呼吸器ジャーナル （(株)医学書院）  72 （ 2 ） 207 - 214 2024年05月

  ISSN  2432-3268

• 気管支拡張症の臨床 レジストリ研究から見えてきたもの

  朝倉 崇徳

  結核 （(一社)日本結核・非結核性抗酸菌症学会）  99 （ 3 ） 91 - 91 2024年05月

  ISSN  0022-9776

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競争的研究費の研究課題 【 表示 ／ 非表示 】

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• 大規模コホートを活用した肺非結核性抗酸菌症の発症機序解明と個別化医療の実現

  2025年07月

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  2028年03月

  令和7年度ゲノム医療実現バイオバンク利活用プログラム（ゲノム医療実現推進プラットフォーム・先端ゲノム研究開発）, 研究代表者

• 肺非結核性抗酸菌症の末梢気道における粘液異常の解明と治療法開発

  2025年04月

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  2028年03月

  日本学術振興会, 科学研究費助成事業, 朝倉 崇徳, 基盤研究(B), 未設定

• 国際連携による気管支拡張症の解剖学的・分子生物学的特性の統合的理解

  2024年09月

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  2028年03月

  日本学術振興会, 科学研究費助成事業, 朝倉 崇徳, 国際共同研究加速基金(海外連携研究), 未設定

• 肺非結核性抗酸菌症患者の宿主疾患感受遺伝子の機能解析による新規治療基盤の創出

  2023年04月

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  2026年03月

  日本学術振興会, 科学研究費助成事業, 南宮 湖, 朝倉 崇徳, 長谷川 直樹, 西村 知泰, 基盤研究(B), 未設定

• 新たな重症呼吸器症候群をきたす感染症に備えた気道部位特異的上皮細胞における分子基盤の創出

  2023年04月

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  2024年03月

  令和4年度 「新興・再興感染症に対する革新的医薬品等開発推進研究事業」, 研究代表者

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• 北里柴三郎記念学術奨励賞

  2025年05月, 日本感染症学会

• 三四会奨励賞

  2024年06月, 慶應義塾大学医学部三四会

• Assembly on Pulmonary Infections & Tuberculosis Rising Star Award for Basic Scientific and/or Translational Research

  2024年05月, 米国胸部疾患学会

• UJA特別賞

  朝倉 崇徳, 2024年04月, 海外日本人研究者ネットワーク

• 学会奨励賞

  朝倉 崇徳, 2024年04月, 日本呼吸器学会

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• フィジカルアセスメントと画像検査

  2025年度

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• フィジカルアセスメントと画像検査

  慶應義塾

  2025年04月

  -

  2026年03月

• 薬学部OSCE評価者

  北里大学薬学部

  2024年12月

• 病態評価学

  北里大学薬学部

  2024年11月

  -

  2024年12月

• フィジカルアセスメントと画像検査

  慶應義塾大学薬学部

  2024年07月

• フィジカルアセスメント実習

  北里大学薬学部

  2024年06月

  -

  2024年07月

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• NPO法人非結核性抗酸菌症・気管支拡張症研究コンソーシアム事務局

  2025年04月

• 徹底解説！-最新版「成人肺非結核性抗酸菌症化学療法に関する見解

  日経メディカルOnline CMEデジタル

  2023年11月

  -

  2023年12月

• 台東区保健所 結核診査会

  2018年04月

  -

  2019年03月

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• 第100回日本結核・非結核性抗酸菌症学会学術講演会 一般演題基礎研究1座長

  2025年06月

• 米国胸部疾患学会2025 Facilitator

  2025年05月

• 第186回日本結核・非結核性抗酸菌症学会/第261回日本呼吸器学会関東地方会セッションⅢ座長

  2024年09月

• 第99回日本結核・非結核性抗酸菌症学会学術講演会 一般演題19基礎研究1座長

  2024年06月

• NTM Host Research Consortium International Workshop 座長

  2022年01月