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dc.contributor.authorAlves, Francisco Acácio-
dc.contributor.authorPelajo-Machado, Marcelo-
dc.contributor.authorTotino, Paulo R. R-
dc.contributor.authorSouza, Mariana T-
dc.contributor.authorGonçalves, Evonnildo Costa-
dc.contributor.authorSchneider, Maria Paula C-
dc.contributor.authorMuniz, José Augusto Pereira Carneiro-
dc.contributor.authorKrieger, Marco A-
dc.contributor.authorAndrade, Marcia C. R-
dc.contributor.authorDaniel-Ribeiro, Cláudio Tadeu-
dc.contributor.authorCarvalho, Leonardo José de Moura-
dc.date.accessioned2020-01-27T16:51:38Z-
dc.date.available2020-01-27T16:51:38Z-
dc.date.issued2015-
dc.identifier.citationALVES, Francisco A. et al. Splenic architecture disruption and parasite-induced splenocyte activation and anergy in Plasmodium falciparum-infected Saimiri sciureus monkeys. Malaria Journal, v. 14, n. 128, p. 1-14, Mar. 2015.pt_BR
dc.identifier.issn1475-2875-
dc.identifier.urihttp://patua.iec.gov.br//handle/iec/4004-
dc.description.abstractBackground: The understanding of the mechanisms of immunity in malaria is crucial for the rational development of interventions such as vaccines. During blood stage infection, the spleen is considered to play critical roles in both immunity and immunopathology of Plasmodium falciparum infections. Methods: Saimiri sciureus monkeys were inoculated with blood stages of P. falciparum (FUP strain) and spleens removed during acute disease (days 7 and 13 of infection) and during convalescence (15 days after start of chloroquine treatment). Cytokine (IFNγ, TNFα, IL2, IL6, IL10, and IL12) responses of splenocytes stimulated with P. falciparum-parasitized red blood cells were assessed by real-time PCR using specific Saimiri primers, and histological changes were evaluated using haematoxylin-eosin and Giemsa-stained slides. Results: Early during infection (day 7, 1-2% parasitaemia), spleens showed disruption of germinal centre architecture with heavy B-cell activation (centroblasts), and splenocytes showed increased expression of IFNγ, IL6 and IL12 upon in vitro stimuli by P. falciparum-parasitized red blood cells (pRBC). Conversely, 15 days after treatment of blood stage infection with chloroquine, splenocytes showed spontaneous in vitro expression of TNFα, IL2, IL6, IL10, and IL12, but not IFNγ, and stimulation with P. falciparum pRBC blocked the expression of all these cytokines. During the acute phase of infection, splenic disarray with disorganized germinal centres was observed. During convalescence, spleens of the chloroquine-treated animals showed white pulp hyperplasia with extensive lymphocyte activation and persistency of heavily haemozoin-laden macrophages throughout the red pulp. Conclusions: Inability to eliminate haemozoin is likely involved in the persistent lymphocyte activation and in the anergic responses of Saimiri splenocytes to P. falciparum pRBC, with important negative impact in immune responses and implications for the design of malaria vaccine.pt_BR
dc.description.sponsorshipThis study was supported by funds from the PDTIS Program (Fiocruz), PRONEX-Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), DECIT-Ministry of Health and and Fundação de Apoio à Pesquisa do Estado do Rio de Janeiro (Faperj).pt_BR
dc.language.isoengpt_BR
dc.publisherBMCpt_BR
dc.rightsAcesso Abertopt_BR
dc.titleSplenic architecture disruption and parasite-induced splenocyte activation and anergy in Plasmodium falciparum-infected Saimiri sciureus monkeyspt_BR
dc.typeArtigopt_BR
dc.subject.decsPrimaryPrimatas / anatomia & histologiapt_BR
dc.subject.decsPrimarySaimiri / anatomia & histologiapt_BR
dc.subject.decsPrimaryMalária Vivax / veterináriapt_BR
dc.subject.decsPrimaryPlasmodium falciparum / isolamento & purificaçãopt_BR
dc.subject.decsPrimaryCitocinas / análisept_BR
dc.creator.affilliationFundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa em Malária. Rio de Janeiro, RJ, Brazil / Universidade Federal do Pará. Laboratório de Imunobiologia. Belém, PA, Brazil.pt_BR
dc.creator.affilliationFundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Patologia. Rio de Janeiro, RJ, Brazil.pt_BR
dc.creator.affilliationFundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa em Malária, Rio de Janeiro, RJ, Brazil.pt_BR
dc.creator.affilliationFundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa em Malária. Rio de Janeiro, RJ, Brazil.pt_BR
dc.creator.affilliationUniversidade Federal do Pará. Laboratório de Tecnologia Biomolecular. Belém, PA, Brazil.pt_BR
dc.creator.affilliationUniversidade Federal do Pará. Laboratório de Polimorfismo de DNA. Belém, PA, Brazil.pt_BR
dc.creator.affilliationMinistério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Centro Nacional de Primatas. Ananindeua, PA, Brasil.pt_BR
dc.creator.affilliationInstituto Carlos Chagas de Biologia Molecular. Curitiba, PR, Brazil.pt_BR
dc.creator.affilliationFundação Oswaldo Cruz. Serviço de Criação de Primatas Não-Humanos. Rio de Janeiro, RJ, Brazil.pt_BR
dc.creator.affilliationFundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa em Malária. Rio de Janeiro, RJ, Brazil.pt_BR
dc.creator.affilliationFundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa em Malária. Rio de Janeiro, RJ, Brazil.pt_BR
dc.identifier.doi10.1186/s12936-015-0641-3-


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