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Air-liquid interphase culture confers SARS-CoV-2 susceptibility to A549 alveolar epithelial cells

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/87072

Title: Air-liquid interphase culture confers SARS-CoV-2 susceptibility to A549 alveolar epithelial cells
Authors: Sasaki, Michihito Browse this author →KAKEN DB
Kishimoto, Mai Browse this author
Itakura, Yukari Browse this author
Tabata, Koshiro Browse this author
Intaruck, Kittiya Browse this author
Uemura, Kentaro Browse this author
Toba, Shinsuke Browse this author
Sanaki, Takao Browse this author
Sato, Akihiko Browse this author
Hall, William W. Browse this author
Orba, Yasuko Browse this author →KAKEN DB
Sawa, Hirofumi Browse this author →KAKEN DB
Keywords: SARS-CoV-2
A549 cells
Air-liquid interface
ACE2
TMPRSS2
Viral entry
Issue Date: Nov-2021
Publisher: Elsevier
Journal Title: Biochemical and biophysical research communications
Volume: 577
Start Page: 146
End Page: 151
Publisher DOI: 10.1016/j.bbrc.2021.09.015
Abstract: The human lung cell A549 is susceptible to infection with a number of respiratory viruses. However, A549 cells are resistant to Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) infection in conventional submerged culture, and this would appear to be due to low expression levels of the SARSCoV-2 entry receptor: angiotensin-converting enzyme-2 (ACE2). Here, we examined SARS-CoV-2 susceptibility to A549 cells after adaptation to air-liquid interface (ALI) culture. A549 cells in ALI culture yielded a layer of mucus on their apical surface, exhibited decreased expression levels of the proliferation marker KI-67 and intriguingly became susceptible to SARS-CoV-2 infection. We found that A549 cells increased the endogenous expression levels of ACE2 and TMPRSS2 following adaptation to ALI culture conditions. Camostat, a TMPRSS2 inhibitor, reduced SARS-CoV-2 infection in ALI-cultured A549 cells. These findings indicate that ALI culture switches the phenotype of A549 cells from resistance to susceptibility to SARS-CoV-2 infection through upregulation of ACE2 and TMPRSS2. (c) 2021 Elsevier Inc. All rights reserved.
Rights: ©2021. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
http://creativecommons.org/licenses/by-nc-nd/4.0/
Type: article (author version)
URI: http://hdl.handle.net/2115/87072
Appears in Collections:人獣共通感染症国際共同研究所 (International Institute for Zoonosis Control) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 佐々木 道仁

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