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Am J Physiol Lung Cell Mol Physiol 280: L134-L140, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 1, L134-L140, January 2001

IL-13 induces mucin production by stimulating epidermal growth factor receptors and by activating neutrophils

Jae Jeong Shim, Karim Dabbagh, Iris F. Ueki, Trang Dao-Pick, Pierre-Regis Burgel, Kiyoshi Takeyama, Dominic Cheng-Wei Tam, and Jay A. Nadel

Cardiovascular Research Institute and Departments of Medicine and Physiology, University of California, San Francisco, California 94132-0130

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-alpha 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.

airway epithelium; mucus hypersecretion; epidermal growth factor receptor activation; T helper 2 cytokine; interleukin


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