ArticleFrontiers in cellular and infection microbiology2021
Fluticasone Propionate Suppresses Poly(I:C)-Induced ACE2 in Primary Human Nasal Epithelial Cells.
Article in Frontiers in cellular and infection microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Differential association of fluticasone furoate and budesonide with clinically detected COVID-19: a retrospective cohort study.BMJ open respiratory research · 2026Article
- Impact of nasal and inhaled corticosteroids on SARS-CoV-2 infection susceptibility.The Journal of allergy and clinical immunology · 2025Article
- Ginsenosides, potential TMPRSS2 inhibitors, a trade-off between the therapeutic combination for anti-PD-1 immunotherapy and the treatment of COVID-19 infection of LUAD patients.Frontiers in pharmacology · 2023Article
- Inhaled corticosteroids for the treatment of COVID-19.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Bioactive components of different nasal spray solutions may defeat SARS-Cov2: repurposing and in silico studies.Journal of molecular modeling · 2022Article
- Reply to "A limitation regarding the association between intranasal corticosteroid use and better COVID-19 outcomes: Nasal symptoms matter".The journal of allergy and clinical immunology. In practice · 2022Article
- ACE2 and Innate Immunity in the Regulation of SARS-CoV-2-Induced Acute Lung Injury: A Review.International journal of molecular sciences · 2021Review
- TLR Signals in Epithelial Cells in the Nasal Cavity and Paranasal Sinuses.Frontiers in allergy · 2021Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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
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