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American Journal of Respiratory Cell and Molecular Biology. Vol. 28, pp. 286-295, 2003
© 2003 American Thoracic Society
DOI: 10.1165/rcmb.4887

Interleukin-9 Induces Goblet Cell Hyperplasia during Repair of Human Airway Epithelia

Paola D. Vermeer*, Robert Harson*, Lisa A. Einwalter, Tom Moninger and Joseph Zabner

Department of General Surgery, Rush-Presbyterian St. Luke's Medical Center, Chicago, Illinois; and Department of Internal Medicine, Central Microscopy Research Facility, University of Iowa, Iowa City, Iowa

Address correspondence to: Joseph Zabner, M.D., University of Iowa College of Medicine, 500 EMRB, Iowa City, IA 52242. E-mail: joseph-zabner{at}uiowa.edu

Asthma is characterized by airway inflammation, smooth muscle hyperreactivity, and airway remodeling with excessive mucus production. The effect cytokines like interleukin (IL)-9 have on airway epithelia has been addressed using murine models of asthma, as well as transgenic and knockout mice. Though highly informative, differences exist between mouse and human airway epithelia, including cellular composition (e.g., Clara cells) and stem cell/plasticity capabilities. Therefore, to address cytokine effects on human airway epithelia, we have used a primary model system to ask whether IL-9 can alter cell fates of human airway epithelia. Here, we show that IL-9 has little effect on fully differentiated ciliated human airway epithelia. However, in the setting of airway injury repair, IL-9 results in goblet cell hyperplasia. A similar response was observed when the epithelium was exposed to IL-9 before it became fully differentiated. Moreover, exposure to IL-9 resulted in increased lysozyme and mucus production by the epithelia. Thus, a combination of IL-9 and mechanical injury can explain, in part, goblet cell hyperplasia that is evident in the lungs of individuals with asthma. These data suggest that interventions that limit airway epithelial damage, block IL-9, or modulate the repair process should result in decreased airway remodeling and prevent the chronic manifestations of this disease.

Abbreviations: diaminobenzidine, DAB • fluorescein isothiocyanate, FITC • interleukin, IL • Jacalin lectin, JAC • periodic acid-Schiff, PAS • phosphate-buffered saline, PBS • scanning electron microscopy, SEM • transmission electron microscopy, TEM




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