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Título: | Overexpression of Glucocorticoid-induced Leucine Zipper (GILZ) increases susceptibility to Imiquimod-induced psoriasis and involves cutaneous activation of TGF-β1 |
Autor: | Carceller, Elena CSIC ORCID; Ballegeer, Marlies; Deckers, Julie; Riccardi, Carlo; Bruscoli, Stefano; Hochepied, Tino; Libert, Claude; Pérez, Paloma CSIC ORCID | Palabras clave: | Chronic inflammation Interleukins Psoriasis Skin diseases |
Fecha de publicación: | 9-dic-2016 | Editor: | Nature Publishing Group | Citación: | Scientific Reports 6:38825 (2016) | Resumen: | Psoriasis vulgaris is a chronic inflammatory skin disease affecting millions of people. Its pathophysiology is complex and involves a skin compartment with epidermal and immune cells which produce cytokines, e.g. belonging to the IL-23-Th17-cell axis. Glucocorticoids (GCs) are the most common therapeutics used in cutaneous inflammatory disorders and GC-induced leucine zipper (GILZ) has emerged as a mediator of GCs due to its anti-inflammatory actions, theoretically lacking GC side-effects. We evaluated whether GILZ may provide a better therapeutic index in comparison to GCs during the onset and progression of psoriasis by generating and characterizing a mouse model with generalized overexpression of this protein (GILZ-Tg mice) and the imiquimod (IMQ) psoriasis model. Unexpectedly, in GILZ-Tg mice, the severity of IMQ-induced psoriasis-like skin lesions as well as induction of cytokines commonly up-regulated in human psoriasis (Il-17, Il-22, Il-23, Il-6, S100a8/a9, and Stat3) was significantly more pronounced relative to GILZ-Wt mice. The increased susceptibility to IMQ-induced psoriasis of GILZ-Tg mice was significantly associated with skin-specific over-activation of TGF-β1-mediated signaling via SMAD2/3. Our findings demonstrate that GILZ may behave as pro-inflammatory protein in certain tissues and that, similar to prolonged GC therapy, GILZ as an alternative treatment for psoriasis may also have adverse effects. | Descripción: | 11 páginas, 6 figuras. Contiene información suplementaria en: http://www.nature.com/srep/ | Versión del editor: | http://dx.doi.org/10.1038/srep38825 | URI: | http://hdl.handle.net/10261/141313 | DOI: | 10.1038/srep38825 | E-ISSN: | 2045-2322 |
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2016 Sci Rep 6-38825.pdf | 1,67 MB | Adobe PDF | Visualizar/Abrir |
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