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Infection of Primary Nasal Epithelial Cells Grown at an Air-Liquid Interface to Characterize Human Coronavirus-Host Interactions
Published on: September 22, 2023
Airway Epithelial-Derived Immune Mediators in COVID-19
Tony J F Guo1, Gurpreet K Singhera1,2, Janice M Leung1,2
1Centre for Heart Lung Innovation, Providence Healthcare Research Institute, St. Paul's Hospital, University of British Columbia, 1081 Burrard St., Vancouver, BC V6Z 1Y6, Canada.
The airway epithelium protects lungs but can cause severe COVID-19 via maladaptive immune responses. Understanding epithelial cells
Area of Science:
- Pulmonology and Immunology
- Cell Biology
- Virology
Background:
- The airway epithelium forms a critical barrier against inhaled pathogens like SARS-CoV-2.
- Epithelial cells initiate immune responses through cytokine and chemokine release.
- Severe COVID-19 involves hyper-inflammation and potential epithelial cell dysfunction.
Purpose of the Study:
- To review airway epithelial barrier and immune functions.
- To examine SARS-CoV-2 interactions with the airway epithelium.
- To discuss epithelial-derived cytokines/chemokines in COVID-19 pathogenesis and as biomarkers.
Main Methods:
- Literature review of studies on airway epithelium, SARS-CoV-2, and immune mediators.
- Analysis of epithelial cell responses to viral infection.
- Exploration of cytokine and chemokine roles in COVID-19.
Main Results:
- Airway epithelium plays a dual role in lung defense and COVID-19 pathogenesis.
- SARS-CoV-2 infection can trigger maladaptive epithelial immune responses.
- Epithelial-derived cytokines and chemokines are implicated in severe COVID-19.
Conclusions:
- The airway epithelium's immune response to SARS-CoV-2 can be detrimental.
- Epithelial dysfunction contributes to hyper-inflammation and disease severity.
- Epithelial-derived immune mediators are potential therapeutic targets for COVID-19.
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