Plasmodium vivax infection alters mitochondrial metabolism in human monocytes

dc.creatorSuelen Queiroz Diniz
dc.creatorFabiano Oliveira
dc.creatorRicardo Tostes Gazzinelli
dc.creatorLis Ribeiro do Valle Antonelli
dc.creatorAndréa Teixeira-carvalho
dc.creatorMaria Marta Figueiredo
dc.creatorPedro Augusto Carvalho Costa
dc.creatorBruno Coelho Rocha
dc.creatorOlindo Assis Martins-filho
dc.creatorRicardo Gonçalves
dc.creatorDhélio Batista Pereira
dc.creatorMauro Shugiro Tada
dc.date.accessioned2023-09-14T19:14:26Z
dc.date.accessioned2025-09-09T01:12:47Z
dc.date.available2023-09-14T19:14:26Z
dc.date.issued2021-07-27
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológico
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais
dc.description.sponsorshipFAPESP - Fundação de Amparo à Pesquisa do Estado de São Paulo
dc.format.mimetypepdf
dc.identifier.doihttps://doi.org/10.1128/mbio.01247-21
dc.identifier.issn2150-7511
dc.identifier.urihttps://hdl.handle.net/1843/58680
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofmBio
dc.rightsAcesso Aberto
dc.subjectMalária
dc.subjectPlasmodium vivax
dc.subjectMetabolismo
dc.subjectMitocôndrias
dc.subjectMonócitos
dc.subjectEspécies Reativas de Oxigênio
dc.subject.otherMalaria
dc.subject.otherP. vivax
dc.subject.otherMetabolism
dc.subject.otherMitochondria
dc.subject.otherMonocytes
dc.subject.otherMitochondrial metabolism
dc.subject.otherReactive oxygen species
dc.titlePlasmodium vivax infection alters mitochondrial metabolism in human monocytes
dc.typeArtigo de periódico
local.citation.epage16
local.citation.issue4
local.citation.spagee01247-21
local.citation.volume12
local.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.
local.identifier.orcidhttps://orcid.org/0000-0003-2427-7699
local.identifier.orcidhttps://orcid.org/0000-0002-4969-8812
local.publisher.countryBrasil
local.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE PATOLOGIA
local.publisher.initialsUFMG
local.url.externahttps://journals.asm.org/doi/10.1128/mbio.01247-21

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