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Updated: Jan 15, 2026

Infection of Primary Nasal Epithelial Cells Grown at an Air-Liquid Interface to Characterize Human Coronavirus-Host Interactions
Published on: September 22, 2023
Barrier dysfunction in nasal epithelium contributes to persistent inflammation in long COVID
Nadia Baalbaki1, Daniëlle van Egmond2, Patricia Jaeger3
1Department of Pulmonary Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; Amsterdam Institute for Infection and Immunity, Amsterdam, The Netherlands; Amsterdam Public Health, Amsterdam, The Netherlands.
Long COVID nasal epithelium dysfunction contributes to immune dysregulation. The IL-1β-IFN-γ axis is a potential therapeutic target for Long COVID (LC) patients.
Area of Science:
- Immunology
- Respiratory Medicine
- Virology
Background:
- Long COVID (LC) involves persistent symptoms linked to chronic inflammation and immune dysregulation.
- Local tissue mechanisms driving LC pathogenesis are not well understood.
Purpose of the Study:
- Investigate the role of the nasal epithelium in Long COVID.
- Determine its contribution to systemic immune activation.
Main Methods:
- Analyzed nasal epithelial and blood samples from LC patients and controls.
- Assessed epithelial barrier function, wound healing, and cytokine profiles.
- Performed RNA sequencing and flow cytometry on innate lymphoid cells (ILCs).
Main Results:
- LC nasal epithelium showed impaired barrier function and reduced expression of ZO-1 and occludin.
- Epithelial repair was reduced despite faster wound closure.
- Increased IL-1β and interferon pathway activation in LC nasal epithelium promoted ILC activation.
Conclusions:
- Nasal epithelial dysfunction and chronic activation in a subgroup of LC patients may drive systemic immune dysregulation.
- The IL-1β-IFN-γ axis is identified as a novel targetable pathway.
- This pathway may inform precision therapies for Long COVID.
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