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Updated: Aug 18, 2025

Infection of Primary Nasal Epithelial Cells Grown at an Air-Liquid Interface to Characterize Human Coronavirus-Host Interactions
Published on: September 22, 2023
Fluticasone propionate suppresses the SARS-CoV-2 induced increase in respiratory epithelial permeability in vitro
K Martens1, E Vanhulle2, A-S Viskens3
1Department of Microbiology, Immunology and Transplantation, Allergy and Clinical Immunology Research Unit, KU Leuven, Leuven, Belgium; Department of Bioscience Engineering, University of Antwerp, Antwerp, Belgium.
Background:
Disruption of the nasal epithelial barrier is believed to play a role in Coronavirus Disease-2019 (COVID-19) outcomes. Fluticasone propionate has been shown to restore the nasal epithelial barrier in allergic rhinitis to the level of healthy controls. The therapeutic potential of nasal steroid sprays in COVID-19 has recently been reported. However, further insight into the mode of action is warranted.
Objectives:
To explore the in vitro mechanisms of the preventive potential of fluticasone propionate in SARS-CoV-2 infection.
Methods:
Human air liquid interface cultures of Calu-3 cells and primary nasal epithelial cells isolated from healthy donors were used to investigate the preventive effect of fluticasone propionate on SARS-CoV-2 induced barrier disruption, virus replication and ACE2 expression.
Results:
48 hours pre-treatment with fluticasone propionate prevented the SARS-CoV-2 induced increase in fluorescein isothiocyanate-dextran 4 kDa permeability and reduced infection with SARS-CoV-2. Pre-treatment with fluticasone propionate also decreased ACE2 expression in SARS-CoV-2 infected Calu-3 cells.
Conclusion:
Fluticasone propionate pre-treatment prevented SARS-CoV-2 increased epithelial permeability, reduced ACE2 expression and SARS-CoV-2 infection, underscoring the therapeutic potential of fluticasone propionate in the context of COVID-19.
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