IL-13 induces mucin production by stimulating epidermal growth factor receptors and by activating neutrophils
- Authors
- Shim J.J.; Dabbagh K.; Ueki I.F.; Dao-Pick T.; Burgel P.-R.; Takeyama K.; Tam D.C.-W.; Nadel J.A.
- Issue Date
- 2001
- Keywords
- Airway epithelium; Epidermal growth factor receptor activation; Interleukin; Mucus hypersecretion; T helper 2 cytokine
- Citation
- American Journal of Physiology - Lung Cellular and Molecular Physiology, v.280, no.1 24-1, pp L134 - L140
- Indexed
- SCOPUS
- Journal Title
- American Journal of Physiology - Lung Cellular and Molecular Physiology
- Volume
- 280
- Number
- 1 24-1
- Start Page
- L134
- End Page
- L140
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/22868
- ISSN
- 1040-0605
1522-1504
- Abstract
- Mucus hypersecretion contributes to the morbidity and mortality in acute asthma. Both T helper 2 (Th2) cytokines and epidermal growth factor receptor (EGFR) signaling have been implicated in allergen-induced goblet cell (GC) metaplasia. Present results show that a cascade of EGFR involving neutrophils is implicated in interleukin (IL)-13-induced mucin expression in GC. Treatment with a selective EGFR tyrosine kinase inhibitor prevented IL-13-induced GC metaplasia dose dependently and completely. Instillation of IL-13 also induced tumor necrosis factor-α protein expression, mainly in infiltrating neutrophils. Control airway epithelium contained few leukocytes, but intratracheal instillation of IL-13 resulted in time-dependent leukocyte recruitment by IL-13-induced IL-8-like chemoattractant expression in airway epithelium. Pretreatment with an inhibitor of leukocytes in the bone marrow (cyclophosphamide) or with a blocking antibody to IL-8 prevented both IL-13-induced leukocyte recruitment and GC metaplasia. These findings indicate that EGFR signaling is involved in IL-13-induced mucin production. They suggest a potential therapeutic role for inhibitors of the EGFR cascade in the hypersecretion that occurs in acute asthma.
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- Appears in
Collections - 2. Clinical Science > Department of Pulmonary, Allergy, and Critical Care Medicine > 1. Journal Articles
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