Anti-inflammatory effect of galectin-1 in a murine model of atopic dermatitis

Atopic dermatitis (ad) is caused by both dysregulated immune responses and an impaired skin barrier. although beta-galactoside-binding protein galectin-1 (gal-1) has immunomodulatory effects in several inflammatory disorders, therapeutic strategies based on its anti-inflammatory properties have not been explored in ad. thus, we evaluate pharmacological treatment with gal-1 in the progression of an ovalbumin (ova)-induced ad-like skin lesions. the skin of ova-immunized 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 recombinant gal-1 (rgal-1) or dexamethasone (dex). 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 eosinophils and mast cells, which was verified by reduced expression of mouse mast cell protease 6 (mmcp6) and eosinophil peroxidase (epx). these localized effects are associated with extracellular signal-regulated kinase (erk) activation and downregulation of endogenous gal-1. the inhibition of disease progression induced by rgal-1 was also correlated with reduced plasma il-17 levels. our results demonstrate that rgal-1 is an effective treatment for allergic skin inflammation in ad and impact the development of novel strategies for skin inflammatory diseases.