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Use este identificador para citar ou linkar para este item: https://repositorio.ufba.br/handle/ri/7763
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dc.contributor.authorAraujo, Maria Ilma Andrade Santos-
dc.contributor.authorBliss, Susan K.-
dc.contributor.authorSuzuki, Yasuhiro-
dc.contributor.authorAlcaraz, Ana-
dc.contributor.authorDenkers, Eric Y.-
dc.contributor.authorPearce, Edward J.-
dc.creatorAraujo, Maria Ilma Andrade Santos-
dc.creatorBliss, Susan K.-
dc.creatorSuzuki, Yasuhiro-
dc.creatorAlcaraz, Ana-
dc.creatorDenkers, Eric Y.-
dc.creatorPearce, Edward J.-
dc.date.accessioned2013-01-04T15:04:52Z-
dc.date.issued2001-03-
dc.identifier.issn0019-9567-
dc.identifier.urihttp://www.repositorio.ufba.br/ri/handle/ri/7763-
dc.descriptionTexto completo: acesso restrito. p. 1454-1462pt_BR
dc.description.abstractWe 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.pt_BR
dc.language.isoenpt_BR
dc.sourcehttp://dx.doi.org/10.1128/IAI.69.3.1454-1462.2001pt_BR
dc.titleInterleukin-12 promotes pathologic liver changes and death in mice coinfected with Schistosoma mansoni and Toxoplasma gondiipt_BR
dc.title.alternativeInfection and Immunitypt_BR
dc.typeArtigo de Periódicopt_BR
dc.identifier.numberv. 69, n. 3pt_BR
dc.embargo.liftdate10000-01-01-
Aparece nas coleções:Artigo Publicado em Periódico (Faculdade de Medicina)

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