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* Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil;
Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil;
Instituto Butantan, São Paulo, Brazil; and
Centre de Recherches Biomedicales des Cordeliers, Université Pierre et Marie Curie, Paris, France
The participation of type I IFNs (IFN-I) in NO production and resistance to Trypanosoma cruzi infection was investigated. Adherent cells obtained from the peritoneal cavity of mice infected by the i.p. route produced NO and IFN-I. Synthesis of NO by these cells was partially inhibited by treatment with anti-IFN-
or anti-TNF- Abs. Compared with susceptible BALB/c mice, peritoneal cells from parasite-infected resistant C57BL/6 mice produced more NO (2-fold), IFN-I (10-fold), and TNF- (3.5-fold). Later in the infection, IFN-I levels measured in spleen cell (SC) cultures from 8-day infected mice were greater in C57BL/6 than in infected BALB/c mice, and treatment of the cultures with anti-IFN- Ab reduced NO production. IFN-
or IL-10 production by SCs was not different between the two mouse strains; IL-4 was not detectable. Treatment of C57BL/6 mice with IFN-I reduced parasitemia levels in the acute phase of infection. Mice deprived of the IFN-R gene developed 3-fold higher parasitemia levels in the acute phase in comparison with control 129Sv mice. Production of NO by peritoneal macrophages and SCs was reduced in mice that lacked signaling by IFN-, whereas parasitism of macrophages was heavier than in control wild-type mice. We conclude that IFN-I costimulate NO synthesis early in T. cruzi infection, which contributes to a better control of the parasitemia in resistant mice.
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1 This investigation was supported by a grant from Fundação de Amparo à Pesquisa do Estado de Sao Paulo and by Conselho Nacional de Pesquisas supplementary fellowships (to I.A.A.). V.M.A.C. was a recipient of Comissao de Aperfeicoamento de Pessoal de Nivel Superior/Programa Institucional de Capacitação Docente e Técnica Ph.D. fellowship, and the experimental work reported herein is part of her doctorate thesis.
2 Current address: Departamento de Medicina Tropical, Universidade Federal de Pernambuco, 50670-901, Recife, PE, Brazil.
3 Address correspondence and reprint requests to Dr. Ises A. Abrahamsohn, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, Avenida Professor Lineu Prestes 1730, 05508-900, São Paulo, SP, Brazil. E-mail address: iabraham{at}usp.br
4 Abbreviations used in this paper: iNOS, inducible NO synthase; IFN-I, type I IFN; HPRT, hypoxanthine-guanine phosphoribosyltransferase; KO, knockout; SC, spleen cell; PC, peritoneal cell; WT, wild type.
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  D. C. Bartholomeu, C. Ropert, M. B. Melo, P. Parroche, C. F. Junqueira, S. M. R. Teixeira, C. Sirois, P. Kasperkovitz, C. F. Knetter, E. Lien, et al. Recruitment and Endo-Lysosomal Activation of TLR9 in Dendritic Cells Infected with Trypanosoma cruzi J. Immunol., July 15, 2008; 181(2): 1333 - 1344. [Abstract] [Full Text] [PDF]
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