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Diniz SQ, Teixeira-Carvalho A, Figueiredo MM, et al. Plasmodium vivax Infection Alters Mitochondrial Metabolism in Human Monocytes. mBio. 2021;12(4):e0124721doi: 10.1128/mBio.01247-21.
Diniz, S. Q., Teixeira-Carvalho, A., Figueiredo, M. M., Costa, P. A. C., Rocha, B. C., Martins-Filho, O. A., Gonçalves, R., Pereira, D. B., Tada, M. S., Oliveira, F., Gazzinelli, R. T., & Antonelli, L. R. D. V. (2021). Plasmodium vivax Infection Alters Mitochondrial Metabolism in Human Monocytes. mBio, 12(4), e0124721. https://doi.org/10.1128/mBio.01247-21
Diniz, Suelen Queiroz, et al. "Plasmodium vivax Infection Alters Mitochondrial Metabolism in Human Monocytes." mBio vol. 12,4 (2021): e0124721. doi: https://doi.org/10.1128/mBio.01247-21
Diniz SQ, Teixeira-Carvalho A, Figueiredo MM, Costa PAC, Rocha BC, Martins-Filho OA, Gonçalves R, Pereira DB, Tada MS, Oliveira F, Gazzinelli RT, Antonelli LRDV. Plasmodium vivax Infection Alters Mitochondrial Metabolism in Human Monocytes. mBio. 2021 Aug 31;12(4):e0124721. doi: 10.1128/mBio.01247-21. Epub 2021 Jul 27. PMID: 34311577; PMCID: PMC8406267.
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mBio. 2021 Aug 31;12(4):e0124721. doi: 10.1128/mBio.01247-21. Epub 2021 Jul 27.

Plasmodium vivax Infection Alters Mitochondrial Metabolism in Human Monocytes.

mBio

Suelen Queiroz Diniz, Andréa Teixeira-Carvalho, Maria Marta Figueiredo, Pedro Augusto Carvalho Costa, Bruno Coelho Rocha, Olindo Assis Martins-Filho, Ricardo Gonçalves, Dhélio Batista Pereira, Mauro Shugiro Tada, Fabiano Oliveira, Ricardo Tostes Gazzinelli, Lis Ribeiro do Valle Antonelli

Affiliations

  1. Instituto René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, Minas Gerais, Brazil.
  2. Instituto de Ciências Biológicas, Departamento de Bioquímica e Imunologia, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
  3. Instituto de Ciências Biológicas, Departamento de Patologia Geral, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
  4. Centro de Pesquisas em Medicina Tropical de Rondônia, Porto Velho, Rondônia, Brazil.
  5. National Institutes of Healthgrid.94365.3d, NIAID, Laboratory of Malaria and Vector Research, Rockville, Maryland, USA.

PMID: 34311577 PMCID: PMC8406267 DOI: 10.1128/mBio.01247-21

Abstract

Monocytes 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.

Keywords: P. vivax; malaria; metabolism; mitochondria; mitochondrial metabolism; monocytes; reactive oxygen species

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