A protective role for IL-13 receptor α 1 in bleomycin-induced pulmonary injury and repair

D. Karo-Atar, A. Bordowitz, O. Wand, M. Pasmanik-Chor, I. E. Fernandez, M. Itan, R. Frenkel, D. R. Herbert, F. D. Finkelman, O. Eickelberg, A. Munitz*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


Molecular mechanisms that regulate lung repair vs. progressive scarring in pulmonary fibrosis remain elusive. Interleukin (IL)-4 and IL-13 are pro-fibrotic cytokines that share common receptor chains including IL-13 receptor (R) α1 and are key pharmacological targets in fibrotic diseases. However, the roles of IL-13Rα1 in mediating lung injury/repair are unclear. We report dysregulated levels of IL-13 receptors in the lungs of bleomycin-treated mice and to some extent in idiopathic pulmonary fibrosis patients. Transcriptional profiling demonstrated an epithelial cell-associated gene signature that was homeostatically dependent on IL-13Rα1 expression. IL-13Rα1 regulated a striking array of genes in the lung following bleomycin administration and Il13ra1 deficiency resulted in exacerbated bleomycin-induced disease. Increased pathology in bleomycin-treated Il13ra1 -/- mice was due to IL-13Rα1 expression in structural and hematopoietic cells but not due to increased responsiveness to IL-17, IL-4, IL-13, increased IL-13Rα2 or type 1 IL-4R signaling. These data highlight underappreciated protective roles for IL-13Rα1 in lung injury and homeostasis.

Original languageEnglish
Pages (from-to)240-253
Number of pages14
JournalMucosal Immunology
Issue number1
StatePublished - 1 Jan 2016


FundersFunder number
FP7 Marie-Curie Reintegration
U.S. Department of Veterans Affairs
Israel Cancer Research Fund
Seventh Framework Programme256311
United States-Israel Binational Science Foundation2009222, 2011244
Fritz Thyssen Stiftung
Israel Science Foundation955/11


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