| First Author | Karo-Atar D | Year | 2016 |
| Journal | Mucosal Immunol | Volume | 9 |
| Issue | 1 | Pages | 240-53 |
| PubMed ID | 26153764 | Mgi Jnum | J:306501 |
| Mgi Id | MGI:6708326 | Doi | 10.1038/mi.2015.56 |
| Citation | Karo-Atar D, et al. (2016) A protective role for IL-13 receptor alpha 1 in bleomycin-induced pulmonary injury and repair. Mucosal Immunol 9(1):240-53 |
| abstractText | 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) alpha1 and are key pharmacological targets in fibrotic diseases. However, the roles of IL-13Ralpha1 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-13Ralpha1 expression. IL-13Ralpha1 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-13Ralpha1 expression in structural and hematopoietic cells but not due to increased responsiveness to IL-17, IL-4, IL-13, increased IL-13Ralpha2 or type 1 IL-4R signaling. These data highlight underappreciated protective roles for IL-13Ralpha1 in lung injury and homeostasis. |
