A malaria experimental por Plasmodium chabaudi chabaudi em camundongo SCID

AUTOR(ES)
DATA DE PUBLICAÇÃO

2003

RESUMO

The NK cells secrete the citoquinas INF-gamma and TNF-alpha - molecules associated with the immune protective mediated by cells of the type Th1 - in response to infection for Plasmodium. Instead the induction of these cells with IL- 12 helps to reduce the mortality by P. chabaudi. Although studies was related the NK cells and its citoquinas play a important role in the control of the malaria, it is known that the genetic factors represent one of the largest determinant of resistance by host infected by Plasmodium sp. For testing the malaria immunity by NK cells, we have used two animal models: the C.B-17 SCID/SCID because their absence of T and B cells and the C57BL/6 animals which are deprived for interferon-gamma gene. In this research, the capacity of both to control the infection was evaluated comparing the parasitaemia among them, using the immunocompetent BALB/c/Uni like a control animal. They were infected intraperitoneally with a dose of 106 parasited red blood cells and the parasitaemia was determined in established intervals for several weeks. So the animals SCID as the animals KO have maintained high parasitemia during chronic phase of the infection. The immunocompetents mice have decreased the parasitemia level , controlling the infection. It could be concluded that the NK cells collaborate to the malaria immunity reducing the parasitaemia; however the data indicating they don t act alone and the resistance against the P. chabaudi could be also a genetic factor. The malaria affects the kidney, not only for the immunocomplex deposition, because the mice C.B17 SCID/SCID/Uni unprovided immunoglobulins also developed renal pathologies: tubular cells exfoliation, thrombosis and necrosis in the glomerulus, also observed in C57BL/6 KO Interferon-gamma animals. It was not observed kidney alterations in C57BL/6 probably because resistant genotype.

ASSUNTO(S)

malaria camundongo parasitologia

ACESSO AO ARTIGO

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