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大学・研究所にある論文を検索できる 「Cell response analysis in SARS-CoV-2 infected bronchial organoids」の論文概要。リケラボ論文検索は、全国の大学リポジトリにある学位論文・教授論文を一括検索できる論文検索サービスです。
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Cell response analysis in SARS-CoV-2 infected bronchial organoids

Sano, Emi Suzuki, Tatsuya Hashimoto, Rina Itoh, Yumi Sakamoto, Ayaka Sakai, Yusuke Saito, Akatsuki Okuzaki, Daisuke Motooka, Daisuke Muramoto, Yukiko Noda, Takeshi Takasaki, Tomohiko Sakuragi, Jun-Ichi Minami, Shohei Kobayashi, Takeshi Yamamoto, Takuya Matsumura, Yasufumi Nagao, Miki Okamoto, Toru Takayama, Kazuo 京都大学 DOI:10.1038/s42003-022-03499-2

2022

概要

The development of an in vitro cell model that can be used to study severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) research is expected. Here we conducted infection experiments in bronchial organoids (BO) and an BO-derived air-liquid interface model (BO-ALI) using 8 SARS-CoV-2 variants. The infection efficiency in BO-ALI was more than 1, 000 times higher than that in BO. Among the bronchial epithelial cells, we found that ciliated cells were infected with the virus, but basal cells were not. Ciliated cells died 7 days after the viral infection, but basal cells survived after the viral infection and differentiated into ciliated cells. Fibroblast growth factor 10 signaling was essential for this differentiation. These results indicate that BO and BO-ALI may be used not only to evaluate the cell response to SARS-CoV-2 and coronavirus disease 2019 (COVID-19) therapeutic agents, but also for airway regeneration studies.

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参考文献

1. Lu, H., Stratton, C. W. & Tang, Y. W. Outbreak of pneumonia of unknown etiology in Wuhan, China: the mystery and the miracle. J. Med. Virol. 92, 401 (2020).

2. Whitworth, J. COVID-19: a fast evolving pandemic. Trans. R. Soc. Tropical Med. Hyg. 114, 241 (2020).

3. Hoffmann, M. et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell 181, 271–280. e278 (2020).

4. Takayama, K. In vitro and animal models for SARS-CoV-2 research. Trends Pharmacol. Sci. 41, 513–517 (2020).

5. Chen, K. G., Park, K., Spence, J. R. Studying SARS-CoV-2 infectivity and therapeutic responses with complex organoids. Nat. Cell Biol. 23, 822–833 (2021).

6. Han, Y. et al. Identification of SARS-CoV-2 inhibitors using lung and colonic organoids. Nature 589, 270–275 (2021).

7. Lamers, M. M. et al. An organoid‐derived bronchioalveolar model for SARS‐ CoV‐2 infection of human alveolar type II‐like cells. EMBO J. 40, e105912 (2021).

8. Van Der Vaart, J. & Clevers, H. Airway organoids as models of human disease. J. Intern. Med. 289, 604–613 (2021).

9. Deguchi, S., Serrano-Aroca, Á., Tambuwala, M. M., Uhal, B. D., Brufsky, A. M. & Takayama, K. SARS-CoV-2 research using human pluripotent stem cells and organoids. Stem Cells Transl. Med. 10, 1491–1499 (2021).

10. Menter, T. et al. Postmortem examination of COVID‐19 patients reveals diffuse alveolar damage with severe capillary congestion and variegated findings in lungs and other organs suggesting vascular dysfunction. Histopathology 77, 198–209 (2020).

11. Rock, J. R., Randell, S. H. & Hogan, B. L. Airway basal stem cells: a perspective on their roles in epithelial homeostasis and remodeling. Dis. Models Mechanisms 3, 545–556 (2010).

12. Morrisey, E. E. Basal cells in lung development and repair. Dev. Cell 44, 653–654 (2018).

13. Yang, Y. et al. Spatial-temporal lineage restrictions of embryonic p63+ progenitors establish distinct stem cell pools in adult airways. Dev. Cell 44, 752–761. e754 (2018).

14. Balasooriya, G. I., Goschorska, M., Piddini, E. & Rawlins, E. L. FGFR2 is required for airway basal cell self-renewal and terminal differentiation. Development 144, 1600–1606 (2017).

15. Yuan, T., Volckaert, T., Chanda, D., Thannickal, V. J. & De Langhe, S. P. Fgf10 signaling in lung development, homeostasis, disease, and repair after injury. Front. Genet. 9, 418 (2018).

16. Beigel, J. H. et al. Remdesivir for the treatment of Covid-19. N. Engl. J. Med. 383, 1813–1826 (2020).

17. Cox, R. M., Wolf, J. D. & Plemper, R. K. Therapeutically administered ribonucleoside analogue MK-4482/EIDD-2801 blocks SARS-CoV-2 transmission in ferrets. Nat. Microbiol. 6, 11–18 (2021).

18. Huh, D., Matthews, B. D., Mammoto, A., Montoya-Zavala, M., Hsin, H. Y. & Ingber, D. E. Reconstituting organ-level lung functions on a chip. Science 328, 1662–1668 (2010).

19. Zhang, M. et al. Biomimetic human disease model of SARS‐CoV‐2‐induced lung injury and immune responses on organ chip system. Adv. Sci. 8, 2002928 (2021).

20. Si, L. et al. A human-airway-on-a-chip for the rapid identification of candidate antiviral therapeutics and prophylactics. Nat. Biomed. Eng. 5, 815–829 (2021). Sun, S.-H. et al. A mouse model of SARS-CoV-2 infection and pathogenesis. Cell Host Microbe 28, 124–133. e124 (2020).

21. Pandey, K., Acharya, A., Mohan, M., Ng, C. L., Reid, S. P. & Byrareddy, S. N. Animal models for SARS‐CoV‐2 research: a comprehensive literature review. Transbound. Emerg. Dis. 68, 1868–1885 (2021).

22. Itoh, N. & Ornitz, D. M. Evolution of the Fgf and Fgfr gene families. TRENDS Genet. 20, 563–569 (2004).

23. Chen, F. & Fine, A. Stem cells in lung injury and repair. Am. J. Pathol. 186, 2544–2550 (2016).

24. Co, J. Y. et al. Controlling epithelial polarity: a human enteroid model for host-pathogen interactions. Cell Rep. 26, 2509–2520. e2504 (2019).

25. Matsuyama, S. et al. Enhanced isolation of SARS-CoV-2 by TMPRSS2- expressing cells. Proc. Natl Acad. Sci. USA 117, 7001–7003 (2020).

26. Ge, S. X., Son, E. W. & Yao, R. iDEP: an integrated web application for differential expression and pathway analysis of RNA-Seq data. BMC Bioinforma. 19, 534 (2018).

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