PT  - JOURNAL ARTICLE
AU  - Frans Eberth Costa Andrade
AU  - Mab Pereira Corrêa
AU  - Alexandre Dantas Gimenes
AU  - Myrna Serapião dos Santos
AU  - Mauro Campos
AU  - Roger Chammas
AU  - José Álvaro Pereira Gomes
AU  - Cristiane Damas Gil
TI  - Galectin-3: role in ocular allergy and potential as a predictive biomarker
AID  - 10.1136/bjophthalmol-2017-311473
DP  - 2018 Jul 01
TA  - British Journal of Ophthalmology
PG  - 1003--1010
VI  - 102
IP  - 7
4099  - http://bjo.bmj.com/content/102/7/1003.short
4100  - http://bjo.bmj.com/content/102/7/1003.full
SO  - Br J Ophthalmol2018 Jul 01; 102
AB  - Aims To evaluate galectin-3 (Gal-3), a β-galactoside binding protein, as a possible biomarker in ocular allergy and further investigated the role of endogenous Gal-3 in a murine model of ovalbumin (OVA)-induced allergic conjunctivitis (AC).Methods Conjunctival impression cytology specimens from control and patients with severe vernal keratoconjunctivitis, treated or untreated, were used to evaluate Gal-3 expression by immunocytochemistry. To investigate the mechanism of action of Gal-3, OVA-immunised BALB/c male wild-type (WT) and Gal-3 null (Gal-3-/-) mice were challenged with eye drops containing OVA on days 14–16 with a subset of animals pretreated with 0.03% tacrolimus (TC) or dexamethasone (Dex).Results Patients with AC and OVA-sensitised WT mice exhibited increased levels of Gal-3 in the conjunctiva compared with control, an effect reverted by the action of Dex and TC therapy. Twenty-four hours after the final OVA challenge, total and anti-OVA IgE levels increased significantly in the blood of OVA-sensitised WT and Gal-3-/- mice compared with controls, supporting the efficacy of the AC model. The lack of endogenous Gal-3 exacerbated the local inflammatory response, increasing the influx of eosinophils and mast cell activation. Additionally, OVA-sensitised Gal-3-/- animals exhibited increased CD4+ expression in the eyes as well as eotaxin, IL-4, IL-13 and interferon-γ levels in the tear fluid compared with WT animals.Conclusion Gal-3 contributes to the pathogenesis of ocular allergy and represents a relevant therapeutic target.