Plasmodium vivax Infection Alters Mitochondrial Metabolism in Human Monocytes
Suelen Queiroz Diniz, Andréa Teixeira‐Carvalho, Maria Marta Figueiredo, Pedro Augusto Carvalho Costa, Bruno Coelho Rocha, Olindo Assis Martins‐Filho, Ricardo Gonçalves, Dhélio B. Pereira, Mauro Shugiro Tada, Fabiano Oliveira, Ricardo T. Gazzinelli, Lis Ribeiro do Valle Antonelli
Abstract
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.