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Am. J. Respir. Cell Mol. Biol., Volume 25, Number 4, October, 2001 474-485

Interleukin-13 Induces Dramatically Different Transcriptional Programs in Three Human Airway Cell Types

June H. Lee,* Naftali Kaminski,* Gregory Dolganov, Gabriele Grunig, Laura Koth, Colin Solomon, David J. Erle, and Dean Sheppard

Lung Biology Center and Center for Occupational and Environmental Health, Cardiovascular Research Institute, and Department of Medicine, University of California, San Francisco, San Francisco, California; Functional Genomics and Institute of Respiratory Medicine, Sheba Medical Center, Tel Hashomer, Israel; Columbia University, St. Luke's-Roosevelt Hospital, New York, New York

Interleukin (IL)-13, a cytokine released by T lymphocytes during immediate hypersensitivity responses, is a central mediator of asthma. Because IL-13 induces phenotypic features of asthma in mice deficient in T and B lymphocytes, it is likely that this cytokine contributes to the development of asthma by acting directly on resident airway cells. To analyze the global effects of IL-13 on gene expression in airway cells that could contribute to the phenotypic features of asthma, we used Genechip HuGene FL arrays (Affymetrix, Santa Clara, CA) that contain probes for approximately 6,500 human genes. Despite activating a common signaling pathway, IL-13 induced dramatically different patterns of gene expression in primary cultures of airway epithelial cells, airway smooth muscle cells, and lung fibroblasts, with little overlap among cell types. The most prominent effects of IL-13 were on airway smooth muscle, but several genes induced in airway epithelial cells and fibroblasts are also candidates that may contribute to phenotypic features of asthma. These results suggest that the in vivo response to IL-13 in the airways likely results from a combination of distinct effects on each of several resident airway cell types.

* Authors denoted contributed equally.
Abbreviations: bronchial smooth muscle cells, BSMCs; complementary DNA, cDNA; cellular RNA, cRNA; dystrophin-associated glycoprotein, DAG; enzyme-linked immunosorbent assay, ELISA; horseradish peroxidase, HRP; interleukin, IL; mitogen-activated protein, MAP; monocyte chemotactic protein-1, MCPs-1; normal human bronchial epithelial cells, NHBEs; normal human lung fibroblasts, NHLFs; phosphate-buffered saline, PBS; reverse-transcriptase/polymerase chain reaction, RT-PCR; sodium dodecyl sulfate polyacrylamide gel electrophoresis, SDS-PAGE; signal transduction and transactivation, STAT; T-cell receptor, TCR.




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