ArticleInternational forum of allergy & rhinology2016
Reversal of cigarette smoke extract-induced sinonasal epithelial cell barrier dysfunction through Nrf2 Activation.
Article in International forum of allergy & rhinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Reduced occludin and claudin-7 expression is associated with urban locations and exposure to second-hand smoke in allergic rhinitis patients.Scientific reports · 2021Trial
- Prediction of future onset of allergic rhinitis and analysis of risk factors in children with food allergy during infancy.European journal of pediatrics · 2026Article
- Nrf2: A Promising Therapeutic Target for Glucocorticoid-Resistant Chronic Rhinosinusitis.Clinical and experimental otorhinolaryngology · 2026Review
- [Research progress in the regulation of allergic rhinitis pathogenesis by the NRF2 pathway].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2025Review
- Deletion of Nrf2 Enhances Susceptibility to Sinonasal Inflammation After Short-Term PMInternational forum of allergy & rhinology · 2025Article
- Change of oral microbiome diversity by smoking across different age groups.Frontiers in microbiology · 2025Article
- Downregulation of TET2 Contributes to Nasal Polypogenesis Through Hypoxia-Inducible Factor 1α-Mediated Epithelial-to-Mesenchymal Transition.Clinical and experimental otorhinolaryngology · 2024Article
- The destruction of mucosal barriers, epithelial remodeling, and impaired mucociliary clearance: possible pathogenic mechanisms of Pseudomonas aeruginosa and Staphylococcus aureus in chronic rhinosinusitis.Cell communication and signaling : CCS · 2023Review
- Article
- Oxidative Stress and Antioxidants in Chronic Rhinosinusitis with Nasal Polyps.Antioxidants (Basel, Switzerland) · 2023Review
- Pathogenesis and treatment of chronic rhinosinusitis from the perspective of sinonasal epithelial dysfunction.Frontiers in medicine · 2023Review
- Particulate matter air pollution exposure disrupts the Nrf2 pathway in sinonasal epithelium via epigenetic alterations in a murine model.International forum of allergy & rhinology · 2022Article
- Nrf2 Activation Protects Against Organic Dust and Hydrogen Sulfide Exposure Induced Epithelial Barrier Loss andFrontiers in cellular and infection microbiology · 2022Article
- Role of Environmental Air Pollution in Chronic Rhinosinusitis.Current allergy and asthma reports · 2021Review
- Disruption of Sinonasal Epithelial Nrf2 Enhances Susceptibility to Rhinosinusitis in a Mouse Model.The Laryngoscope · 2021Article
- Allyl isothiocyanate increases MRP1 expression in cigarette smoke extract-stimulated human bronchial epithelial cells via the JNK/Nrf2 pathway.Experimental and therapeutic medicine · 2021Article
- Airway Epithelial Dynamics in Allergy and Related Chronic Inflammatory Airway Diseases.Frontiers in cell and developmental biology · 2020Review
- Deletion of Nrf2 enhances susceptibility to eosinophilic sinonasal inflammation in a murine model of rhinosinusitis.International forum of allergy & rhinology · 2019Article
- Aeroallergens, air pollutants, and chronic rhinitis and rhinosinusitis.World journal of otorhinolaryngology - head and neck surgery · 2018Review
- Characterization of a novel, papain-inducible murine model of eosinophilic rhinosinusitis.International forum of allergy & rhinology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundEnvironmental factors such as inhaled pollutants like cigarette smoke may play a significant role in diseases of the upper airway including chronic rhinosinusitis (CRS). Recent studies have shown that cigarette smoke causes impaired airway epithelial cell barrier function likely through environmental oxidative stress related pathways. The purpose of this study is to explore whether enhancing nuclear factor erythroid 2 [NF-E2]-related factor 2 [Nrf2], the body's master antioxidant system, can ameliorate cigarette smoke-induced sinonasal epithelial cell (SNEC) barrier dysfunction.
methodsHuman SNECs (HSNECs) were grown from control patients at the air-liquid interface (ALI). HSNECs were stimulated with cigarette smoke extract (CSE) with and without pharmacologic activation of Nrf2. HSNECs were then stained for the epithelial cell junctional proteins zonula occludens 1 (ZO-1) and junctional adhesion molecule A (JAM-A) using confocal microscopy. In addition, transepithelial electrical resistance (TER) was measured in cultures before and after stimulation with CSE.
resultsCSE stimulation caused a global disruption of the epithelial junctional proteins ZO-1 and JAM-A along with an associated decrease in TER levels. Enhancing Nrf2 levels prior to stimulation with CSE was associated with increased localization of ZO-1 and JAM-A levels at the cell surface and statistically significant increases in TER levels.
conclusionThis is the first study to demonstrate that cigarette smoke induced SNEC barrier dysfunction is reversible by Nrf2 activation. The Nrf2 antioxidant pathway may represent a potential therapeutic target for cigarette smoke-associated sinonasal inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.