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Use este identificador para citar ou linkar para este item: https://repositorio.ufba.br/handle/ri/7763
Tipo: Artigo de Periódico
Título: Interleukin-12 promotes pathologic liver changes and death in mice coinfected with Schistosoma mansoni and Toxoplasma gondii
Título(s) alternativo(s): Infection and Immunity
Autor(es): Araujo, Maria Ilma Andrade Santos
Bliss, Susan K.
Suzuki, Yasuhiro
Alcaraz, Ana
Denkers, Eric Y.
Pearce, Edward J.
Autor(es): Araujo, Maria Ilma Andrade Santos
Bliss, Susan K.
Suzuki, Yasuhiro
Alcaraz, Ana
Denkers, Eric Y.
Pearce, Edward J.
Abstract: We previously demonstrated that mice concurrently infected withSchistosoma mansoni and Toxoplasma gondiiundergo accelerated mortality which is preceded by severe liver damage. Abnormally high levels of serum tumor necrosis factor alpha (TNF-α) in the dually infected mice suggested a role for this and related proinflammatory mediators in the pathologic alterations. In order to evaluate the factors involved in increased inflammatory-mediator production and mortality, interleukin-12−/−(IL-12−/−) mice were coinfected with S. mansoni and T. gondii, and survival and immune responses were monitored. These IL-12−/− mice displayed decreased liver damage and prolonged time to death relative to wild-type animals also coinfected with these parasites. Relative to the response of cells from the coinfected wild-type animals, levels of TNF-α, gamma interferon, and NO produced by splenocytes from coinfected IL-12−/− mice were reduced, and levels of IL-5 and IL-10 were increased, with the net result that the immune response of the dually infected IL-12−/− mice was similar to that of the wild-type mice infected with S. mansoni alone. While dually infected wild-type animals succumb in the absence of overt parasitemia, the delayed death in the absence of IL-12 is associated with relatively uncontrolled T. gondii replication. These data support the view that S. mansoni-infected mice are acutely sensitive to infection with T. gondii as a result of their increased hepatic sensitivity to high levels of proinflammatory cytokines; IL-12 and TNF-α are implicated in this process.
URI: http://www.repositorio.ufba.br/ri/handle/ri/7763
Data do documento: Mar-2001
Aparece nas coleções:Artigo Publicado em Periódico (Faculdade de Medicina)

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