Atopic dermatitis (AD) is caused by both dysregulated immune Key messages & Pharmacological treatment with rGal-1 reduces clinical responses and an impaired skin barrier. Although beta- galactoside-binding protein galectin-1 (Gal-1) has immuno- signs of atopic dermatitis. & Systemic treatment with rGal-1 inhibits eosinophil and modulatory effects in several inflammatory disorders, therapeu- mast cell influx in the skin of AD animals. tic strategies based on its anti-inflammatory properties have not been explored in AD. Thus, we evaluate pharmacological treat- & rGal-1 reduced local eotaxin levels and systemic IL-17 levels. ment with Gal-1 in the progression of an ovalbumin (OVA)- induced AD-like skin lesions. The skin of OVA-immunized & The inhibition of disease progression induced by rGal-1 was correlated with upregulation of phosphorylated ERK. male BALB/c mice was challenged with drops containing OVA on days 11, 14–18 and 21–24. Additionally, in the last . . . week, a subset of animals was treated intraperitoneally with Keywords Galectin-1 Skin inflammation Ovalbumin . . recombinant Gal-1 (rGal-1) or dexamethasone (Dex). Eosinophil Mast cell ERK Treatment with rGal-1 decreased the clinical signs of dermatitis in BALB/c mice and diminished local eotaxin and IFN-γ levels. The treatment also suppressed the infiltration of eosin- Introduction ophils
Journal of Molecular Medicine – Springer Journals
Published: Jun 29, 2017
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