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Identification of pendrin as a common mediator for mucus production in bronchial asthma and chronic obstructive pulmonary disease
- Source :
- Scopus-Elsevier
- Publication Year :
- 2008
-
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.
- Subjects :
- Male
Neutrophils
medicine.medical_treatment
Immunology
Respiratory Mucosa
Mucin 5AC
Pathogenesis
Mice
Pulmonary Disease, Chronic Obstructive
Mediator
Th2 Cells
Chlorocebus aethiops
otorhinolaryngologic diseases
medicine
Immunology and Allergy
Animals
Humans
Lung
Asthma
Aged
COPD
Interleukin-13
biology
business.industry
Genome, Human
Mucins
Membrane Transport Proteins
Epithelial Cells
Pendrin
respiratory system
Middle Aged
medicine.disease
Mucus
respiratory tract diseases
Disease Models, Animal
Cytokine
Neutrophil Infiltration
Sulfate Transporters
COS Cells
biology.protein
Female
business
Airway
Subjects
Details
- ISSN :
- 00221767
- Volume :
- 180
- Issue :
- 9
- Database :
- OpenAIRE
- Journal :
- Journal of immunology (Baltimore, Md. : 1950)
- Accession number :
- edsair.doi.dedup.....05359be12f472a79e32d2b9ff24e1b03