title: Different infective forms trigger distinct immune response in experimental Chagas disease.
abstract: Although 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 proinflammatory cytokine TNF-α and later of IFN-γ 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-γ, 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.
authors.affiliation: Laboratório de Imunopatologia, Núcleo de Pesquisas em Ciências Biológicas (NUPEB), Universidade Federal de Ouro Preto (UFOP), Ouro Preto, Minas Gerais, Brazil.
authors.forename: Paula Melo de Abreu
authors.initials: PM
authors.lastname: Vieira
authors.forename: Amanda Fortes
authors.initials: AF
authors.lastname: Francisco
authors.forename: Evandro Marques de Meneses
authors.initials: EM
authors.lastname: Machado
authors.forename: Nívia Carolina
authors.initials: NC
authors.lastname: Nogueira
authors.forename: Kátia da Silva
authors.initials: Kda S
authors.lastname: Fonseca
authors.forename: Alexandre Barbosa
authors.initials: AB
authors.lastname: Reis
authors.forename: Andrea
authors.initials: A
authors.lastname: Teixeira-Carvalho
authors.forename: Olindo Assis
authors.initials: OA
authors.lastname: Martins-Filho
authors.forename: Washington Luiz
authors.initials: WL
authors.lastname: Tafuri
authors.forename: Cláudia Martins
authors.initials: CM
authors.lastname: Carneiro
mesh_terms: D000818:Animals; D014355:Chagas Disease / Q000276:immunology* / Q000469:parasitology*; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D006790:Host-Parasite Interactions / Q000276:immunology; D016130:Immunophenotyping; D007962:Leukocytes / Q000276:immunology; D051379:Mice; D009205:Myocarditis / Q000276:immunology / Q000469:parasitology / Q000473:pathology; D018512:Parasitemia / Q000276:immunology; D013154:Spleen / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D013997:Time Factors; D014349:Trypanosoma cruzi / Q000276:immunology*
chemical_list: D016207:Cytokines