Different infective forms trigger distinct immune response in experimental Chagas disease

dc.creatorVieira, Paula Melo de Abreu
dc.creatorFrancisco, Amanda Fortes
dc.creatorMachado, Evandro Marques de Menezes
dc.creatorNogueira, Nívia Carolina
dc.creatorFonseca, Katia da Silva
dc.creatorReis, Alexandre Barbosa
dc.creatorCarvalho, Andréa Teixeira de
dc.creatorMartins Filho, Olindo Assis
dc.creatorTafuri, Washington Luiz
dc.creatorCarneiro, Cláudia Martins
dc.date2014-02-18T12:37:39Z
dc.date2014-02-18T12:37:39Z
dc.date2012
dc.date.accessioned2023-09-27T00:15:09Z
dc.date.available2023-09-27T00:15:09Z
dc.identifierABREU VIEIRA, Paula Melo ET AL. Different infective forms trigger distinct immune response in experimental Chagas disease. Plos One. 2012; 7(3)e32912
dc.identifier1932-6203
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/7317
dc.identifier10.1371/journal.pone.0032912
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8898974
dc.descriptionAlthough metacyclic and blood trypomastigotes are completely functional in relation to parasite-host interaction and/or target cell invasion, they differ in the molecules present on the surface. Thus, aspects related to the variability that the forms of T. cruzi interacts with host cells may lead to fundamental implications on the immune response against this parasite and, consequently, the clinical evolution of Chagas disease. We have shown that BT infected mice presented higher levels of parasitemia during all the acute phase of infection. Moreover, the infection with either MT or BT forms resulted in increased levels of total leukocytes, monocytes and lymphocytes, specifically later for MT and earlier for BT. The infection with BT forms presented earlier production of pro inflammatory cytokine TNF- a and later of IFN-c by both T cells subpopulations. This event was accompanied by an early cardiac inflammation with an exacerbation of this process at the end of the acute phase. On the other hand, infection with MT forms result in an early production of IFN-c , with subsequent control in the production of this cytokine by IL-10, which provided to these animals an immunomodulatory profile in the end of the acute phase. These results are in agreement with what was found for cardiac inflammation where animals infected with MT forms showed intense cardiac inflammation later at infection, with a decrease in the same at the end of this phase. In summary, our findings emphasize the importance of taking into account the inoculums source of T. cruzi , since vectorial or transfusional routes of T. cruzi infection may trigger distinct parasite-host interactions during the acute phase that may influence relevant biological aspects of chronic Chagas disease
dc.formatapplication/pdf
dc.languageeng
dc.publisherPublic Library of Science
dc.rightsopen access
dc.subjectChagas disease
dc.titleDifferent infective forms trigger distinct immune response in experimental Chagas disease
dc.typeArticle


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