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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/58680
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dc.creatorSuelen Queiroz Dinizpt_BR
dc.creatorFabiano Oliveirapt_BR
dc.creatorRicardo Tostes Gazzinellipt_BR
dc.creatorLis Ribeiro do Valle Antonellipt_BR
dc.creatorAndréa Teixeira-carvalhopt_BR
dc.creatorMaria Marta Figueiredopt_BR
dc.creatorPedro Augusto Carvalho Costapt_BR
dc.creatorBruno Coelho Rochapt_BR
dc.creatorOlindo Assis Martins-filhopt_BR
dc.creatorRicardo Gonçalvespt_BR
dc.creatorDhélio Batista Pereirapt_BR
dc.creatorMauro Shugiro Tadapt_BR
dc.date.accessioned2023-09-14T19:14:26Z-
dc.date.available2023-09-14T19:14:26Z-
dc.date.issued2021-07-27-
dc.citation.volume12pt_BR
dc.citation.issue4pt_BR
dc.citation.spagee01247-21pt_BR
dc.citation.epage16pt_BR
dc.identifier.doihttps://doi.org/10.1128/mbio.01247-21pt_BR
dc.identifier.issn2150-7511pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/58680-
dc.description.resumoMonocytes play an important role in the host defense against Plasmodium vivax as the main source of inflammatory cytokines and mitochondrial reactive oxygen species (mROS). Here, we show that monocyte metabolism is altered during human P. vivax malaria, with mitochondria playing a major function in this switch. The process involves a reprograming in which the cells increase glucose uptake and produce ATP via glycolysis instead of oxidative phosphorylation. P. vivax infection results in dysregulated mitochondrial gene expression and in altered membrane potential leading to mROS increase rather than ATP production. When monocytes were incubated with P. vivax-infected reticulocytes, mitochondria colocalized with phagolysosomes containing parasites representing an important source mROS. Importantly, the mitochondrial enzyme superoxide dismutase 2 (SOD2) is simultaneously induced in monocytes from malaria patients. Taken together, the monocyte metabolic reprograming with an increased mROS production may contribute to protective responses against P. vivax while triggering immunomodulatory mechanisms to circumvent tissue damage. IMPORTANCE Plasmodium vivax is the most widely distributed causative agent of human malaria. To achieve parasite control, the human immune system develops a substantial inflammatory response that is also responsible for the symptoms of the disease. Among the cells involved in this response, monocytes play an important role. Here, we show that monocyte metabolism is altered during malaria, with its mitochondria playing a major function in this switch. This change involves a reprograming process in which the cells increase glucose uptake and produce ATP via glycolysis instead of oxidative phosphorylation. The resulting altered mitochondrial membrane potential leads to an increase in mitochondrial reactive oxygen species rather than ATP. These data suggest that agents that change metabolism should be investigated and used with caution during malaria.pt_BR
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológicopt_BR
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Geraispt_BR
dc.description.sponsorshipFAPESP - Fundação de Amparo à Pesquisa do Estado de São Paulopt_BR
dc.format.mimetypepdfpt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE PATOLOGIApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofmBiopt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectMalariapt_BR
dc.subjectP. vivaxpt_BR
dc.subjectMetabolismpt_BR
dc.subjectMitochondriapt_BR
dc.subjectMonocytespt_BR
dc.subjectMitochondrial metabolismpt_BR
dc.subjectReactive oxygen speciespt_BR
dc.subject.otherMaláriapt_BR
dc.subject.otherPlasmodium vivaxpt_BR
dc.subject.otherMetabolismopt_BR
dc.subject.otherMitocôndriaspt_BR
dc.subject.otherMonócitospt_BR
dc.subject.otherEspécies Reativas de Oxigêniopt_BR
dc.titlePlasmodium vivax infection alters mitochondrial metabolism in human monocytespt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://journals.asm.org/doi/10.1128/mbio.01247-21pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-2427-7699pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-4969-8812pt_BR
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