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Galectin-3: role in ocular allergy and potential as a predictive biomarker
  1. Frans Eberth Costa Andrade1,
  2. Mab Pereira Corrêa2,
  3. Alexandre Dantas Gimenes1,
  4. Myrna Serapião dos Santos3,
  5. Mauro Campos3,
  6. Roger Chammas4,
  7. José Álvaro Pereira Gomes3,
  8. Cristiane Damas Gil1,2
  1. 1Departamento de Morfologia e Genética, UNIFESP—Universidade Federal de São Paulo, Sao Paulo, Brazil
  2. 2Programa de Pós-Graduação em Biociências, Instituto de Biociências, Letras e Ciências Exatas, UNESP—Universidade Estadual Paulista, Sao Jose do Rio Preto, Brazil
  3. 3Departamento de Oftalmologia e Ciências Visuais, UNIFESP—Universidade Federal de São Paulo, Sao Paulo, Brazil
  4. 4Departamento de Radiologia e Oncologia, FMUSP—Faculdade de Medicina da Universidade de São Paulo and Instituto do Câncer do Estado de São Paulo, Sao Paulo, Brazil
  1. Correspondence to Dr Cristiane Damas Gil, Departamento de Morfologia e Genética, UNIFESP -Universidade Federal de São Paulo, São Paulo 04023-900, Brazil; cristiane.gil{at}unifesp.br

Abstract

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.

  • keratoconjunctivitis
  • impression cytology
  • galectin
  • eosinophil
  • mast cell

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Footnotes

  • Contributors FECA and CDG performed the experiments. All authors contributed to the sample collection and data analysis/interpretation. FECA and CDG wrote the manuscript. All authors have reviewed and approved the final version of manuscript. CDG conceived and designed the study.

  • Funding FECA was supported by Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES).

  • Competing interests None declared.

  • Patient consent Obtained.

  • Ethics approval Ethical Committee of Federal University of São Paulo (CEP nº 1.151.068)

  • Provenance and peer review Not commissioned; externally peer reviewed.

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