Identification of pendrin as a common mediator for mucus production in bronchial asthma and chronic obstructive pulmonary disease
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Updated: Jul 5, 2026
Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
Isao Nakao1, Sachiko Kanaji, Shoichiro Ohta
1Department of Biomolecular Sciences, Saga Medical School, Saga, Japan.
Abstract:
Excessive production of airway mucus is a cardinal feature of bronchial asthma and chronic obstructive pulmonary disease (COPD) and contributes to morbidity and mortality in these diseases. IL-13, a Th2-type cytokine, is a central mediator in the pathogenesis of bronchial asthma, including mucus overproduction. Using a genome-wide search for genes induced in airway epithelial cells in response to IL-13, we identified pendrin encoded by the SLC26A4 (PDS) gene as a molecule responsible for airway mucus production. In both asthma and COPD mouse models, pendrin was up-regulated at the apical side of airway epithelial cells in association with mucus overproduction. Pendrin induced expression of MUC5AC, a major product of mucus in asthma and COPD, in airway epithelial cells. Finally, the enforced expression of pendrin in airway epithelial cells in vivo, using a Sendai virus vector, rapidly induced mucus overproduction in the lumens of the lungs together with neutrophilic infiltration in mice. These findings collectively suggest that pendrin can induce mucus production in airway epithelial cells and may be a therapeutic target candidate for bronchial asthma and COPD.
Insights
Pendrin, a protein encoded by the SLC26A4 gene, drives mucus production in airway diseases like asthma and COPD. Targeting pendrin may offer new therapeutic strategies for these conditions.
Area of Science:
- Respiratory Medicine
- Molecular Biology
- Immunology
Background:
- Excessive airway mucus is a key feature of asthma and COPD, contributing to disease severity.
- Interleukin-13 (IL-13) is a critical mediator in asthma pathogenesis, particularly mucus overproduction.
Purpose of the Study:
- To identify genes responsible for IL-13-induced mucus production in airway epithelial cells.
- To investigate the role of pendrin (encoded by SLC26A4) in airway mucus hypersecretion.
Main Methods:
- Genome-wide gene expression analysis in response to IL-13.
- In vivo studies using asthma and COPD mouse models.
- In vivo gene transfer using a Sendai virus vector to enforce pendrin expression.
Main Results:
- Pendrin was identified as an IL-13-induced gene in airway epithelial cells.
- Pendrin expression was upregulated in airway epithelial cells in asthma and COPD mouse models, correlating with mucus overproduction.
- Enforced pendrin expression in vivo led to rapid mucus overproduction and neutrophilic infiltration.
Conclusions:
- Pendrin plays a significant role in inducing airway mucus production.
- Pendrin is a potential therapeutic target for managing mucus hypersecretion in asthma and COPD.
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