期刊
BRITISH JOURNAL OF OPHTHALMOLOGY
卷 102, 期 7, 页码 1003-1010出版社
BMJ PUBLISHING GROUP
DOI: 10.1136/bjophthalmol-2017-311473
关键词
keratoconjunctivitis; impression cytology; galectin; eosinophil; mast cell
资金
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
Aims To evaluate galectin-3 (Gal-3), a -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-fourhours 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- 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.
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