ArticleERJ open research2025
SARS-CoV-2 spike treatment and transfection impairs airway epithelial repair.
Article in ERJ open research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Characterizing airway epithelial cultures grown on permeable inserts with different pore densities.Physiological reports · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The airway epithelium serves as a physical and immune barrier against inhaled insults. This tissue is susceptible to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and, following injury, the airway epithelium undergoes repair to restore barrier function. Although components of SARS-CoV-2, such as the spike glycoprotein essential in viral entry, have been shown to alter biological functions in various tissues, it is unclear how SARS-CoV-2 can impact airway epithelial functions, such as wound repair. Methods: In this study, 16HBE14o- epithelial monolayer cultures were either treated with recombinant SARS-CoV-2 spike glycoprotein S1 subunit at 4 μg·mL Results: Spike treatment and transfection altered measures of culture proliferation and markers of proliferation and cell cycle arrest. Secreted interleukin-6 but not interleukin-8 were significantly higher with spike S1 treatment, while both were significantly elevated with spike transfection. Wound closure was inhibited by both spike treatment and transfection, with significant reductions compared to control. Conclusions: SARS-CoV-2 spike S1 treatment and transfection can alter measures of proliferation and inflammation as well as impair wound closure of 16HBE14o- airway epithelial cells. These results highlight how components of SARS-CoV-2 can impair functions of the airway epithelium independent of viral replication.
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Registered trials
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