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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

BALB/c and C57BL/6 Mice Cytokine Responses to Trypanosoma cruzi Infection Are Independent of Parasite Strain Infectivity

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Autor(es):
Ferreira, Bianca L. [1] ; Ferreira, Eden R. [1] ; de Brito, Marlon V. [2] ; Salu, Bruno R. [2] ; Oliva, Maria L. V. [2] ; Mortara, Renato A. [1] ; Orikaza, Cristina M. [1]
Número total de Autores: 7
Afiliação do(s) autor(es):
[1] Univ Fed Sao Paulo, Escola Paulista Med, Dept Microbiol Imunol & Parasitol, Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, Escola Paulista Med, Dept Bioquim, Sao Paulo - Brazil
Número total de Afiliações: 2
Tipo de documento: Artigo Científico
Fonte: FRONTIERS IN MICROBIOLOGY; v. 9, MAR 26 2018.
Citações Web of Science: 4
Resumo

Trypanosoma cruzi is the etiologic agent of Chagas' disease, which affects 6-7 million people worldwide. Different strains of T. cruzi present specific genotypic and phenotypic characteristics that affect the host-pathogen interactions, and thus, the parasite has been classified into six groups (TcI to TcVI). T. cruzi infection presents two clinical phases, acute and chronic, both with distinct characteristics and important participation by the immune system. However, the specific contributions of parasite and host factors in the disease phases are not yet fully understood. The murine model for Chagas' disease is well-established and reproduces important features of the human infection, providing an experimental basis for the study of host lineages and parasite strains. Thus, we evaluated acute and chronic infection by the G (TcI) and CL (TcVI) strains of T. cruzi, which have distinct tropisms and infectivity, in two inbred mice lineages (C57BL/6 and BALB/c) that display variable degrees of susceptibility to different T. cruzi strains. Analysis of the parasite loads in host tissues by qPCR showed that CL strain established an infection faster than the G strain; at the same time, the response in BALB/c mice, although diverse in terms of cytokine secretion, was initiated earlier than that in C57BL/6 mice. At the parasitemia peak in the acute phase, we observed, either by confocal microscopy or by qPCR, that the infection was disseminated in all groups analyzed, with some differences concerning parasite tropism; at this point, all animals responded to infection by increasing the serum concentrations of cytokines. However, BALB/c mice seemed to better regulate the immune response than C57BL/6 mice. Indeed, in the chronic phase, C57BL/6 mice still presented exacerbated cytokine and chemokine responses. In summary, our results indicate that in these experimental models, the deregulation of immune response that is typical of chronic Chagas' disease may be due to control loss over pro-and anti-inflammatory cytokines early in the acute phase of the disease, depending primarily on the host background rather than the parasite strain. (AU)

Processo FAPESP: 14/21338-2 - Avaliação in loco da infecção aguda e crônica por tripomastigotas de Trypanosoma cruzi (TCI e TcVI) em camundongos isogênicos BALB/c e C57BL/6
Beneficiário:Bianca Rodrigues Lima Ferreira
Linha de fomento: Bolsas no Brasil - Mestrado
Processo FAPESP: 11/51475-3 - Biologia molecular e celular do parasitismo por Trypanosoma cruzi
Beneficiário:José Franco da Silveira Filho
Linha de fomento: Auxílio à Pesquisa - Temático