This is the first study to demonstrate that HDM-induced SNEC barrier dysfunction may be preventable by Nrf2 activation. Enhancing Nrf2 activation through treatment with SFN prior to stimulation with HDM was associated with increased localization of ZO-1 at the cell surface and statistically significant increases in TER ( p < 0.05) and decrease in paracellular FITC-dextran permeability ( p < 0.001).
IL-33 levels were determined by real-time polymerase chain reaction (PCR) and by immunochemical staining with anti-IL-33 antibody. After exposure to either HMGB1 or ATP in vitro, SNECs were processed for messenger RNA (mRNA) extraction and immunocytochemistry. HDM stimulation caused a global disruption of the protein ZO-1 along with an associated decrease in TER ( p < 0.001) and increased FITC-dextran paracellular permeability ( p < 0.0001). Tissue was prepared for immunohistochemistry and for SNEC air-liquid interface culture. Transepithelial electrical resistance (TER) and paracellular fluorescein isothiocyanate (FITC)-dextran permeability was measured in response to stimulation with HDM and SFN. Allergens such as house dust mite (HDM) have been reported to disrupt SNEC barrier integrity. HSNECs were then stained for the epithelial cell junction protein zonula occludens-1 (ZO-1) and cell surface localization was evaluated by confocal microscopy. Dysregulated sinonasal epithelial cell (SNEC) barrier function has been proposed to contribute to the pathogenesis of sinonasal inflammatory conditions such as allergic rhinitis (AR) and chronic rhinosinusitis (CRS).
HSNECs were stimulated with HDM with or without pharmacologic activation of Nrf2 with SFN. But a new local study by re searchers from SNEC and SERI may potentially help doctors detect the eye disease at an earlier stage. Field of view is one’s entire scope of vision, which includes the central and side vision. Human SNECs (HSNECs) were grown from patients at the air-liquid interface (ALI). ophthalmologist at SNEC’s Glaucoma Department. The purpose of this study was to explore whether Nrf2 activation could ameliorate HDM-induced SNEC barrier dysfunction. We have recently identified nuclear erythroid 2-related factor 2 (Nrf2) activation via sulforaphane (SFN) stimulation to stabilize SNEC barrier function. Moreover, SNECs originating in the head and neck region have been reported to be highly aggressive and to have a poor prognosis. Allergens such as house dust mite (HDM) have been reported to disrupt SNEC barrier integrity. Primary small cell neuroendocrine carcinoma (SNEC) of the paranasal sinuses is an extremely rare and distinctive tumor with aggressive clinical behavior. Dysregulated sinonasal epithelial cell (SNEC) barrier function has been proposed to contribute to the pathogenesis of sinonasal inflammatory conditions such as allergic rhinitis (AR) and chronic rhinosinusitis (CRS).
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