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Study of galectin-9 in experimental atopical dermatitis treated or not with dexamethasone

Grant number: 17/10610-1
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): November 01, 2017
Effective date (End): October 31, 2019
Field of knowledge:Biological Sciences - Morphology - Histology
Principal researcher:Cristiane Damas Gil
Grantee:Libnah Leal Areias
Home Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil


Galectin-9 (Gal-9) belongs to a protein family characterized by a conserved carbohydrate recognition domain (CRD) of approximately 135 amino acids responsible for its binding to ²-galactoside sugars. In experimental models of inflammation, Gal-9 has been pointed as an anti-inflammatory mediator. However, in relation to its mechanisms of action in allergy, Gal-9 can play a dual role, either regulating or activating the cellular response. Thus, we will evaluate the expression pattern of Gal-9 and its relationship with inflammatory cells in ovalbumin (OVA)-induced experimental atopic dermatitis in mice. The experimental procedures were approved by the Ethics Committee in Animal Experimentation of the Federal University of São Paulo - UNIFESP (CEUA nº 1906060115/2015). Four experimental groups (n = 6 animals/group) will be evaluated: NAÏVE, SHAM, DA (atopic dermatitis), and DA+DEX (atopic dermatitis treated with dexamethasone). Male Balb/c mice were immunized with a subcutaneous injection of ovalbumin (OVA; 5 µg) in the days 0 and 7. After immunization, mice was challenged with 250 µg OVA diluted in 50 µl of Johnson's Baby ® oil, in the days 11, 14 to 18 and 21 to 24. Part of the sensitized mice was treated with rGal-1 by intraperitoneal injection (0,3 or 3 µg/mice) or dexamethasone (1 mg/kg) diluted in 0.1 mL of sterile saline, in the last week of the protocol, days 21 to 24 (once a day). After 24 hours of the last OVA challenge, or just oil (Sham), mice were euthanized to skin collection. Studies will be conducted through: I) histological analysis and quantification of inflammatory cells; II) localization and possible modulation of Gal-9 expression in the skin through immunohistochemistry, immunofluorescence and western blotting. The results will contribute to a better understanding of the cellular and molecular mechanisms that involve the biological actions of Gal-9 in the allergy, as well as possible therapeutic targets for the skin inflammatory processes. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
CORREA, MAB P.; AREIAS, LIBNAH L.; CORREIA-SILVA, REBECA D.; D'AVILA, SOLANGE C. G. P.; LEOPOLDINO, ANDREIA M.; GRECO, KARIN V.; GIL, CRISTIANE D.. The Role of Galectin-9 as Mediator of Atopic Dermatitis: Effect on Keratinocytes. CELLS, v. 10, n. 4, . (17/26872-5, 17/10610-1)

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