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

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

Mucosal Immunol. 9, 240-253 (2016)
Verlagsversion DOI PMC
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 1933-0219
e-ISSN 1933-0219
Zeitschrift Mucosal Immunology
Quellenangaben Band: 9, Heft: 1, Seiten: 240-253 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Verlagsort UNITED STATES
Begutachtungsstatus