ArticleToxicological sciences : an official journal of the Society of Toxicology2022
Perfluorooctane Sulfonic Acid Disrupts Protective Tight Junction Proteins via Protein Kinase D in Airway Epithelial Cells.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 48 citations in OpenAlex.
- Early Life Exposure to PFOS or F‑53B is Associated with Increased Asthma Susceptibility in Offspring and Alterations in the Pulmonary Barrier, Immune Function, and Gut Microbiota.Environment & health (Washington, D.C.) · 2026Article
- Current Status of Per- and Poly-Fluoroalkyl Substances (PFAS) Exposure on Lung Cell Biology and Pulmonary Outcomes along Human Health Risk Assessment Steps.Current allergy and asthma reports · 2026Review
- Perfluorohexanoic acid (PFHxA) induces cytochrome P450 expression and enzymatic activity in well-differentiated primary human bronchial epithelial (HBE) cells.The Science of the total environment · 2026Article
- PPAR-gamma regulates PFAS-mediated proinflammatory cytokines in lung epithelial cells.Frontiers in pharmacology · 2026Article
- PFAS exposure and reproductive dysfunction: implications for outcomes in assisted reproductive technologies.Frontiers in endocrinology · 2026Review
- KIF1B Regulates NLRP3-Mediated Pyroptosis in Asthma Progression.Journal of cellular and molecular medicine · 2025Article
- Review
- Identification of Novel Lactylation-Related Biomarkers for COPD Diagnosis Through Machine Learning and Experimental Validation.Biomedicines · 2025Article
- Specific Ambient PMEnvironmental science & technology · 2025Article
- New insights into the effects of PFOS exposure on rat lung development: morphological, functional, and single-cell sequencing analysis.Archives of toxicology · 2025Article
- Developmental perfluorooctane sulfonic acid exposure exacerbates house dust mite induced allergic responses in adult mice.The Science of the total environment · 2024Article
- Characterizing PFAS hazards and risks: a human population-based in vitro cardiotoxicity assessment strategy.Human genomics · 2024Article
- Developmental PFOS exposure alters lung inflammation and barrier integrity in juvenile mice.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Per- and poly-fluoroalkyl substances (PFAS) effects on lung health: a perspective on the current literature and future recommendations.Frontiers in toxicology · 2024Review
- Assessment of the metabolome across the glucose tolerance spectrum in adults with cystic fibrosis hospitalized for pulmonary exacerbations.Respiratory medicineArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Perfluorooctane sulfonic acid (PFOS) is a long chain per- and polyfluoroalklyl substance (PFAS) that has been used in aqueous film-forming foams. Emerging epidemiological evidence indicates that PFOS may be associated with chronic lung diseases such as asthma and analysis of human tissues demonstrates that the lungs carry a significant body burden of PFOS. Deficits in barrier function are a major risk factor for asthma. Thus, we hypothesized that PFOS exposure will lead to impaired epithelial barrier function through dysregulated tight junctions. Hence, we assessed the impact of PFOS on epithelial barrier integrity. Bronchial epithelial cells (16HBE) were grown on collagen-coated transwells and treated to 5-25 μM PFOS, and assessed for changes in barrier function and tight junction proteins. Rescue experiments were performed using the protein kinase D (PKD) inhibitor, CID755673. PFOS treatment reduced transepithelial electrical resistance (TEER) and increased 4 kDa FITC-dextran flux. Additionally, PFOS significantly decreased protein levels and the tight junction organization rate of occludin and zonula occludens 1. Increased phosphorylation (Ser744/Ser748) of PKD was observed 3 h following PFOS treatment. Pretreatment with the PKD inhibitor attenuated PFOS-mediated changes in TEER and FITC-dextran flux and restored occludin protein levels. In conclusion, PFOS causes loss of airway barrier integrity and the disruption of tight junctions in bronchial epithelial cells, which was partly attenuated through the inhibition of PKD. These findings demonstrate that PFOS is capable of disrupting airway barrier function, a potentially driving factor underlying associations between PFOS and respiratory diseases such as asthma.
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