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Infection of Primary Nasal Epithelial Cells Grown at an Air-Liquid Interface to Characterize Human Coronavirus-Host Interactions
Published on: September 22, 2023
Interleukin-33 induces mucin gene expression and goblet cell hyperplasia in human nasal epithelial cells
Hajime Ishinaga1, Masako Kitano1, Masaaki Toda2
1Department of Otorhinolaryngology-Head & Neck Surgery, Mie University Graduate School of Medicine, Japan.
Abstract:
We investigated whether IL-33 is involved in mucus overproduction and goblet cell hyperplasia in eosinophilic chronic rhinosinusitis (ECRS). IL-33 mRNA was significantly higher in the eosinophilic CRS group than in the non-eosinophilic CRS group from human nasal polyps. IL-33 induced MUC5AC mRNA and MUC5AC protein, and also goblet cell hyperplasia at air liquid interface culture in human nasal epithelial cells. In addition to that, IL-33 induced MUC5B and FOXA3, and reduces FOXJmRNA. In conclusion, our present study demonstrated that the direct evidence of IL-33 which lead to increase mucin gene and protein expression, as well as goblet cell hyperplasia. This study provides novel insights into the role of IL-33 on mucus overproduction in eosinophilic inflammation of human airways.
Insights
Interleukin-33 (IL-33) drives mucus overproduction and goblet cell hyperplasia in eosinophilic chronic rhinosinusitis (ECRS). This finding reveals IL-33
Area of Science:
- Immunology
- Respiratory Medicine
- Molecular Biology
Background:
- Eosinophilic chronic rhinosinusitis (ECRS) is characterized by airway inflammation and mucus hypersecretion.
- The precise molecular mechanisms driving mucus overproduction in ECRS require further elucidation.
Purpose of the Study:
- To investigate the role of Interleukin-33 (IL-33) in mucus overproduction and goblet cell hyperplasia in ECRS.
Main Methods:
- Quantitative analysis of IL-33 mRNA levels in human nasal polyps from ECRS patients.
- In vitro air-liquid interface culture of human nasal epithelial cells to assess IL-33's effects on mucin gene and protein expression.
- Evaluation of goblet cell hyperplasia following IL-33 stimulation.
Main Results:
- Significantly elevated IL-33 mRNA levels were observed in eosinophilic CRS compared to non-eosinophilic CRS.
- IL-33 stimulation led to increased MUC5AC mRNA and protein expression.
- IL-33 induced goblet cell hyperplasia and altered the expression of other key genes (MUC5B, FOXA3, FOXJ1).
Conclusions:
- IL-33 directly promotes mucin gene and protein expression, contributing to mucus overproduction in ECRS.
- This study provides direct evidence for IL-33's role in goblet cell hyperplasia and mucus dysregulation in eosinophilic airway inflammation.
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