ArticleInternational forum of allergy & rhinology2019
Deletion of Nrf2 enhances susceptibility to eosinophilic sinonasal inflammation in a murine model of rhinosinusitis.
Article in International forum of allergy & rhinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Oxidative stress and reactive oxygen species in otorhinolaryngological diseases: insights from pathophysiology to targeted antioxidant therapies.Redox report : communications in free radical research · 2025Review
- Deletion of Nrf2 Enhances Susceptibility to Sinonasal Inflammation After Short-Term PMInternational forum of allergy & rhinology · 2025Article
- Mitochondrial dynamics modulate the allergic inflammation in a murine model of allergic rhinitis.Immunity, inflammation and disease · 2023Article
- The Effects of Wildfire Smoke on Asthma and Allergy.Current allergy and asthma reports · 2023Review
- Oxidative Stress and Air Pollution: Its Impact on Chronic Respiratory Diseases.International journal of molecular sciences · 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
- Isoorientin ameliorates OVA-induced asthma in a murine model of asthma.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Disruption of Sinonasal Epithelial Nrf2 Enhances Susceptibility to Rhinosinusitis in a Mouse Model.The Laryngoscope · 2021Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundOxidative stress exacerbates lower airway diseases including asthma and chronic obstructive pulmonary disease (COPD); however, its role in upper airway (sinonasal) chronic inflammatory disorders is less clear. Nuclear erythroid 2 p45-related factor (Nrf2) is an endogenous mechanism that upon activation invokes an antioxidant response pathway via nuclear translocation and upregulation of cytoprotective genes. We sought to determine whether deletion of Nrf2 enhances susceptibility to allergic sinonasal inflammation in vivo.
methodsNrf2
resultsWe show that deletion of Nrf2 results in enhances indices of allergen-induced sinonasal inflammation including aggravated eosinophil accumulation and goblet cell hyperplasia. An exaggerated increase in epithelial derived inflammatory cytokines including interleukin 33 (IL-33) and thymic stromal lymphopoietin (TSLP) was observed in the nasal lavage fluid and sinonasal mucosal tissue of Nrf2
conclusionThese data show that the endogenous Nrf2 pathway limits Ova-induced sinonasal inflammation, epithelial derived inflammatory cytokine production, and epithelial barrier dysfunction in vivo and identify a potential therapeutic target in the management of allergic sinonasal inflammatory disorders. This is the first study to our knowledge which shows that Nrf2 regulates allergic inflammation in the sinonasal cavity in vivo.
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