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Galectin-3 is essential for reactive oxygen species production by peritoneal neutrophils from mice infected with a virulent strain of Toxoplasma gondii

Published online by Cambridge University Press:  14 September 2012

C. M. O. S. ALVES
Affiliation:
Laboratory of Immunoparasitology, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Av. Pará 1720, 38400-902, Uberlândia, MG, Brazil
D. A. O. SILVA
Affiliation:
Laboratory of Immunoparasitology, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Av. Pará 1720, 38400-902, Uberlândia, MG, Brazil
A. E. C. S. AZZOLINI
Affiliation:
Laboratory of Immunochemistry, Department of Physics and Chemistry, Universidade de São Paulo, Av. do Café s/no, 14040-903, Ribeirão Preto, SP, Brazil
C. M. MARZOCCHI-MACHADO
Affiliation:
Department of Clinical, Toxicological and Bromatological Analyses, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Av. do Café s/no, 14040-903, Ribeirão Preto, SP, Brazil
Y. M. LUCISANO-VALIM
Affiliation:
Laboratory of Immunochemistry, Department of Physics and Chemistry, Universidade de São Paulo, Av. do Café s/no, 14040-903, Ribeirão Preto, SP, Brazil
M. C. ROQUE-BARREIRA
Affiliation:
Laboratory of Glycobiology, Department of Molecular and Cellular Biology and Pathogenic Bioagents, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Av. dos Bandeirantes 3900, 14049-900, Ribeirão Preto, SP, Brazil
J. R. MINEO*
Affiliation:
Laboratory of Immunoparasitology, Institute of Biomedical Sciences, Universidade Federal de Uberlândia, Av. Pará 1720, 38400-902, Uberlândia, MG, Brazil
*
*Corresponding author: Laboratório de Imunoparasitologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Av. Pará 1720, Campus Umuarama, 38400-902, Uberlândia, MG, Brazil. Tel: +55 34 3218 2058. Fax: +55 34 3218 2333. E-mail: [email protected]

Summary

Toxoplasma gondii stimulates a potent pro-inflammatory response and neutrophils are involved in early infection. Galectin-3 (Gal-3) is an endogenous modulator of inflammatory processes and anti-infective agents, but its interaction with neutrophils in T. gondii infection is still unclear. Here, we evaluated the role of Gal-3 in peritoneal inflammation, reactive oxygen species (ROS) production by neutrophils and survival, after in vivo T. gondii infection with virulent RH strain, using Gal-3 deficient and wild type mice. Animals were inoculated with thioglycollate or tachyzoites, and peritoneal cells were harvested for analysis of the influx of leukocytes. Neutrophils were isolated from peritoneal exudates from infected mice and stimulated with phorbol myristate acetate (PMA) to evaluate ROS production by luminol-dependent chemiluminescence assay. Our results showed that: (1) Gal-3 upregulates peritoneal inflammation, with enhanced recruitment of neutrophils and lymphocytes after thioglycollate stimulation, but does not influence the enhanced neutrophil influx after early T. gondii infection; (2) Gal-3 upregulates ROS generation by inflammatory peritoneal neutrophils from infected mice, but downregulates its production in non-infected mice and (3) Gal-3 does not influence the survival of mice after infection with the virulent T. gondii strain. In conclusion, Gal-3 is essential for ROS generation by neutrophils in the initial acute phase of T. gondii infection and this phenomenon may constitute an attempt to control parasite growth during in vivo infection with the T. gondii virulent strain.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2012

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