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Fluticasone Propionate Suppresses Poly(I:C)-Induced ACE2 in Primary Human Nasal Epithelial Cells

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Title: Fluticasone Propionate Suppresses Poly(I:C)-Induced ACE2 in Primary Human Nasal Epithelial Cells
Authors: Nakazono, Akira Browse this author
Nakamaru, Yuji Browse this author
Ramezanpour, Mahnaz Browse this author
Kondo, Takeshi Browse this author
Watanabe, Masashi Browse this author
Hatakeyama, Shigetsugu Browse this author
Kimura, Shogo Browse this author
Honma, Aya Browse this author
Wormald, P. J. Browse this author
Vreugde, Sarah Browse this author
Suzuki, Masanobu Browse this author →KAKEN DB
Homma, Akihiro Browse this author →KAKEN DB
Keywords: SARS-CoV-2
virus infection
toll-like receptors
intranasal steroid spray
Issue Date: 26-Apr-2021
Publisher: Frontiers Media
Journal Title: Frontiers in Cellular and Infection Microbiology
Volume: 11
Start Page: 655666
Publisher DOI: 10.3389/fcimb.2021.655666
Abstract: Background From the first detection in 2019, SARS-CoV-2 infections have spread rapidly worldwide and have been proven to cause an urgent and important health problem. SARS-CoV-2 cell entry depends on two proteins present on the surface of host cells, angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). The nasal cavity is thought to be one of the initial sites of infection and a possible reservoir for dissemination within and between individuals. However, it is not known how the expression of these genes is regulated in the nasal mucosa. Objective In this study, we examined whether the expression of ACE2 and TMPRSS2 is affected by innate immune signals in the nasal mucosa. We also investigated how fluticasone propionate (FP), a corticosteroid used as an intranasal steroid spray, affects the gene expression. Methods Primary human nasal epithelial cells (HNECs) were collected from the nasal mucosa and incubated with Toll-like receptor (TLR) agonists and/or fluticasone propionate (FP), followed by quantitative PCR, immunofluorescence, and immunoblot analyses. Results Among the TLR agonists, the TLR3 agonist Poly(I:C) significantly increased ACE2 and TMPRSS2 mRNA expression in HNECs (ACE2 36.212 +/- 11.600-fold change, p<0.0001; TMPRSS2 5.598 +/- 2.434-fold change, p=0.031). The ACE2 protein level was also increased with Poly(I:C) stimulation (2.884 +/- 0.505-fold change, p=0.003). The Poly(I:C)-induced ACE2 expression was suppressed by co-incubation with FP (0.405 +/- 0.312-fold change, p=0.044). Conclusion The activation of innate immune signals via TLR3 promotes the expression of genes related to SARS-CoV2 cell entry in the nasal mucosa, although this expression is suppressed in the presence of FP. Further studies are required to evaluate whether FP suppresses SARS-CoV-2 viral cell entry.
Type: article
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

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