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Updated: Oct 27, 2025

Infection of Primary Nasal Epithelial Cells Grown at an Air-Liquid Interface to Characterize Human Coronavirus-Host Interactions
Published on: September 22, 2023
Viral stimulation modulates endotype-related ACE2 expression in eosinophilic chronic rhinosinusitis
1Department of Otorhinolaryngology, Seoul National University College of Medicine, Boramae Medical Center, Seoul, Republic of Korea; Sensory Organ Research Institute, Seoul National University Medical Research Center.
Eosinophilic chronic rhinosinusitis (CRS) shows lower ACE2 expression, but viral stimulation upregulates ACE2 and TMPRSS2 in these tissues. This impacts SARS-CoV-2 entry in CRS patients.
Area of Science:
- Immunology
- Virology
- Rhinology
Background:
- Angiotensin-converting enzyme 2 (ACE2) is a key SARS-CoV-2 receptor highly expressed in nasal mucosa.
- Chronic rhinosinusitis (CRS) has diverse endotypes and is worsened by viral infections.
- The influence of viral stimulation and CRS endotype on ACE2 expression is not well understood.
Purpose of the Study:
- To investigate ACE2 and TMPRSS2 expression in relation to CRS endotypes.
- To assess the impact of viral stimulation (poly[I:C]) and cytokines on ACE2/TMPRSS2 expression.
- To understand the cellular mechanisms of SARS-CoV-2 entry in different CRS subtypes.
Main Methods:
- Evaluated ACE2 and TMPRSS2 expression across CRS phenotypes, endotypes, and tissue types.
- Correlated ACE2/TMPRSS2 levels with inflammatory mediators in nasal polyps.
- Utilized air-liquid interface cultures of primary epithelial cells from healthy, eosinophilic NP (ENP), and non-eosinophilic NP (NENP) for stimulation experiments.
Main Results:
- Interleukin-13 (IL-13) reduced ACE2 but increased TMPRSS2 expression in nasal epithelial cells.
- Eosinophilic CRS (ENP) exhibited lower ACE2 expression compared to non-eosinophilic CRS (NENP).
- Viral stimulation (poly[I:C]) combined with IL-13 upregulated ACE2 and TMPRSS2 in ENP tissues.
Conclusions:
- Eosinophilic CRS tissues demonstrate reduced ACE2 expression.
- Viral stimulation can enhance ACE2 and TMPRSS2 expression in eosinophilic CRS.
- Findings suggest viral entry mechanisms in CRS are endotype-dependent.
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