Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/9922
Title: Experimental Trypanosoma cruzi infection in platelet-activating factor receptor-deficient mice.
Authors: Talvani, André
Santana, Gilcinea
Barcelos, Lucíola da Silva
Ishii, Satoshi
Shimizu, Takao
Romanha, Álvaro José
Silva, João Santana da
Soares, Milena Botelho Pereira
Teixeira, Mauro Martins
Affilliation: Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brasil
Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brasil
Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brasil
University of Tokyo. Faculty of Medicine. Department of Biochemistry and Molecular Biology. Tokyo, Japan / CREST of Japan Science and Technology Corporation. Tokyo, Japan
University of Tokyo. Faculty of Medicine. Department of Biochemistry and Molecular Biology. Tokyo, Japan / CREST of Japan Science and Technology Corporation. Tokyo, Japan
Fundação Oswaldo Cruz. Centro de Pesquisa René Rachou. Belo Horizonte, MG, Brasil
Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto. Ribeirão Preto, SP, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Belo Horizonte, MG, Brasil / Fundação Oswaldo Cruz. Centro de Pesquisa René Rachou. Belo Horizonte, MG, Brasil
Abstract: The generation of an inflammatory response driven by Trypanosoma cruzi or its subproducts appears to be essential for tissue injury and disease pathogenesis. However, this inflammatory response is also relevant in the control of T. cruzi replication. The lipid mediator platelet-activating factor (PAF) has been implicated in a number of pathological conditions characterized by tissue inflammation. In the present study, we aimed at evaluating the role of PAF during T. cruzi infection by using mice that were genetically deficient in the PAF receptor. We observed that infected hearts of PAFR(-/-) mice had an increased number of parasite nests, associated with a more intense inflammatory infiltrate. This was associated with greater parasitemia and lethality. When wild-type and PAFR(-/-) mice were compared, there were no marked changes in the kinetics of the expression of MCP-1, RANTES, IFN-gamma and TNF-alpha in heart tissue of infected animals. Moreover, serum concentrations of TNF-alpha, nitrate and parasite-specific IgM were similar in both groups of mice. In vitro, macrophages from PAFR(-/-) animals did not phagocytose trypomastigote forms when activated with PAF, leukotriene B(4) or MCP-1 and produced less nitric oxide when infected and activated with IFN-gamma. These results are consistent with the hypothesis that endogenous synthesis of PAF and activation of PAF receptors control T. cruzi replication in mice in great part via facilitation of the uptake of the parasite and consequent activation of macrophages
Keywords: Platelet-activating factor
Protozoan infection
Inflammation
Chemokines
TNF-a
Knockout
DeCS: Cardiomiopatia Chagásica/imunologia
Fator de Ativação de Plaquetas/fisiologia
Glicoproteínas da Membrana de Plaquetas/fisiologia
Receptores de Superfície Celular/fisiologia
Trypanosoma cruzi/crescimento & desenvolvimento
Anticorpos Antiprotozoários/sangue
Animais
Células Cultivadas
Cardiomiopatia Chagásica/metabolismo
Cardiomiopatia Chagásica/parasitologia
Quimiocina CCL2/biossíntese
Feminino
Coração/parasitologia
Imunoglobulina M/sangue
Interferon gama/biossíntese
Leucotrieno B4/farmacologia
Macrófagos/parasitologia
Camundongos
Issue Date: 2003
Publisher: Elsevier
Citation: TALVANI, A. et al. Experimental Trypanosoma cruzi infection in platelet-activating factor receptor-deficient mice. Microbes and Infection, v. 5, n. 9, p. 789-796, 2003.
DOI: 10.1016/S1286-4579(03)00146-1
ISSN: 1286-4579
Copyright: open access
Appears in Collections:BA - IGM - Artigos de Periódicos

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