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PAGES: 561-568 DOI: 10.1590/0074-02760160529 Full paper
Protection mediated by chemokine CXCL10 in BALB/c mice infected by Leishmania infantum

Webertty Mayk Eufrásio Figueiredo1, Sayonara de Melo Viana1, Dorotheia Teixeira Alves1, Priscila Valera Guerra1, Zirlane Castelo Branco Coêlho2, Helene Santos Barbosa3, Maria Jania Teixeira1,+

1Universidade Federal do Ceará, Faculdade de Medicina, Departamento de Patologia e Medicina Legal, Fortaleza, CE, Brasil
2Universidade Federal do Ceará, Faculdade de Farmácia, Odontologia e Enfermagem, Departamento de Análise Clínica, Fortaleza, CE, Brasil
3Fundação Oswaldo Cruz-Fiocruz, Instituto Oswaldo Cruz, Laboratório de Biologia Estrutural, Rio de Janeiro, RJ, Brasil


BACKGROUND Visceral leishmaniasis (VL) caused by Leishmania infantum is characterised by the loss of the ability of the host to generate an effective immune response. Chemokines have a direct involvement in the pathogenesis of leishmaniasis, causing a rapid change in the expression of these molecules during infection by Leishmania.

OBJECTIVES Herein, it was investigated the role of CXCL10 in controlling infection by L. infantum.

METHODS RAW 264.7 macrophages were infected with L. infantum in vitro and treated or not with CXCL10 (25, 50 and 100 ng/mL). Parasite load, as well as nitric oxide (NO), IL-4 and IL-10 production were assessed at 24 and 48 h after infection. In vivo, BALB/c mice were infected and treated or not with CXCL10 (5 μg/kg) at one, three and seven days of infection. Parasite load, IFN-g, IL-4, TGF-β and IL-10 were evaluated one, seven and 23 days post treatment.

FINDINGS In vitro, CXCL10 reduced parasitic load, not dependent on NO, and inhibited IL-10 and IL-4 secretion. In vivo, CXCL10 was able to reduce the parasite load in both liver and spleen, four weeks after infection, representing a higher decrease in the number of parasites in these organs, also induced IFN-γ at day 23 after treatment, correlating with the decrease in parasite load, and reduced IL-10 and TGF-β.

MAIN CONCLUSIONS This study suggests a partial protective role of CXCL10 against L. infantum, mediated by IFN-g, not dependent on NO, and with suppression of IL-10 and TGF-β. These data may provide information for the development of new approaches for future therapeutic interventions for VL.

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Financial support: CNPq, CAPES, CAPES-Programa DINTER (Doutorado Interinstitucional) Medicina Tropical 309/2013.
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Received 12 December 2016
Accepted 4 March 2017