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Interleukin-13 Stimulates the Proliferation of Lung Myofibroblasts via a Signal Transducer and Activator of Transcription-6-Dependent Mechanism*: A Possible Mechanism for the Development of Airway Fibrosis in Asthma

Jennifer L. Ingram, PhD; Annette Rice, BS; Kristen Geisenhoffer, BS; David K. Madtes, MD; James C. Bonner, PhD
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*From the Laboratory of Pulmonary Pathobiology (Drs. Ingram and Bonner, Ms. Rice, and Ms. Geisenhoffer), National Institute of Environmental Health Science, Research Triangle Park, NC; and Fred Hutchinson Cancer Research Center (Dr. Madtes), Seattle, WA.

Correspondence to: James C. Bonner, PhD, the National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709; e-mail: bonnerj@niehs.nih.gov



Chest. 2003;123(3_suppl):422S-424S. doi:10.1378/chest.123.3_suppl.422S
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Subepithelial fibrosis is increasingly recognized as a component of airway remodeling during the pathogenesis of asthma. It is well known that the airway fibrotic response is due to myofibroblast proliferation and the subsequent deposition of collagen by these cells.1 However, it is unclear which soluble factors initiate and perpetuate the growth of myofibroblasts surrounding small airways. Interleukin (IL)-13, a T helper type 2 cytokine, has been proposed as a major mediator of airway remodeling in asthma patients.2 IL-13 levels are elevated in the lungs of patients with asthma and pulmonary fibrosis.3 Furthermore, the overexpression of IL-13 in murine lungs results in an asthma-like phenotype that includes airway fibrosis.4 Many of the effects of IL-13 are mediated via the transcription factor STAT-6, and mice deficient in STAT-6 are protected from IL-13-induced airway remodeling.5 Although the pathology of IL-13-induced airway remodeling has been well-characterized, little is known regarding the effect of IL-13 on myofibroblast growth. In this study, we investigated IL-13 as a possible mitogen for lung myofibroblasts.

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