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Updated: Nov 20, 2025
07:40
Determining Ciliary Function and Membrane Impermeability of the Pseudostratified Lung Airway Epithelium
Published on: February 21, 2025
987
Titanium dioxide particles modulate epithelial barrier protein, Claudin 7 in asthma
Yun-Gi Lee1, Sun-Hye Lee1, Jisu Hong1
1Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, 170 Jomaru-ro, Wonmi-gu, Bucheon, 14584, Republic of Korea.
Molecular Immunology
|January 23, 2021
Summary
Titanium dioxide (TiO2) exposure impairs airway epithelial barrier function, reducing Claudin-7 (CLDN7) levels and worsening asthma symptoms. This highlights TiO2
Area of Science:
- Pulmonary immunology
- Environmental health
- Epithelial biology
Background:
- Epithelial barrier dysfunction is a key factor in allergic inflammation and asthma.
- Claudins (CLDNs), particularly CLDN7, regulate epithelial permeability but their role in asthma is unclear.
- Inhaled allergens and air pollutants can compromise airway barrier integrity.
Purpose of the Study:
- To investigate the impact of titanium dioxide (TiO2) exposure on epithelial barrier function in asthma.
- To assess the effect of TiO2 on Claudin-7 (CLDN7) expression and related signaling pathways.
- To examine CLDN7 levels in patients with asthma.
Main Methods:
- Murine model of asthma (OVA sensitization/challenge) and TiO2 exposure.
- ELISA, immunoblotting, and immunohistochemistry to analyze CLDN7 levels.
- Human bronchial epithelial cells (NHBE) treated with TiO2 and house dust mite (HDM) extracts.
- Measurement of trans-epithelial electrical resistance (TEER) and Western blot for p-AKT and p-ERK.
Main Results:
- CLDN7 levels were lower in plasma from asthma patients and associated with disease severity.
- Asthma increased CLDN7 expression in mouse lungs and NHBE cells, but TiO2 exposure suppressed it.
- TiO2 exposure reduced p-AKT and p-ERK levels in asthmatic mice and NHBE cells.
- TiO2 and HDM extracts individually increased TEER, but combined treatment decreased it, indicating barrier disruption.
Conclusions:
- Particulate matter, like TiO2, contributes to airway epithelial barrier dysfunction.
- TiO2 exposure may exacerbate asthma by disrupting CLDN7 expression and signaling pathways.
- Airway epithelial barrier impairment is a significant mechanism linking environmental pollutants to asthma pathogenesis.
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