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The CD14CD16 Inflammatory Monocyte Subset Displays Increased Mitochondrial Activity and Effector Function During Acute Malaria
Malaria, caused by a protozoa parasite, Plasmodium, affects more than 200 million people per year. The infection triggers an acute febrile illness, the paroxysms, occurring every 48 or 72 hours depending on the species. Plasmodium vivax, in most cases, does not cause severe malaria, but it is the most geographically widespread parasite responsible for human disease and causes substantial costs to individuals and governments. Once the parasite reaches the blood stream, they infect reticulocytes that can be destroyed by phagocytes. Our goal was to assess the importance of monocyte subsets during malaria. We found that P. vivax infection causes an increase in frequency of circulating monocytes, which were defined as classical, inflammatory, and patrolling, based on the expression of membrane molecules. Classical and inflammatory monocytes produced higher levels of pro-inflammatory cytokines and were distinguished from patrolling monocytes by displaying larger and more active mitochondria. Importantly, inflammatory monocytes were more efficient phagocytes; produced high levels of intracellular reactive oxygen species and TNF and consequently control better Plasmodium vivax infection. Hence, our results support the hypothesis that CD14+CD16+ monocytes display effector functions involved in parasite control during malaria.
Vyšlo v časopise: The CD14CD16 Inflammatory Monocyte Subset Displays Increased Mitochondrial Activity and Effector Function During Acute Malaria. PLoS Pathog 10(9): e32767. doi:10.1371/journal.ppat.1004393
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004393Souhrn
Malaria, caused by a protozoa parasite, Plasmodium, affects more than 200 million people per year. The infection triggers an acute febrile illness, the paroxysms, occurring every 48 or 72 hours depending on the species. Plasmodium vivax, in most cases, does not cause severe malaria, but it is the most geographically widespread parasite responsible for human disease and causes substantial costs to individuals and governments. Once the parasite reaches the blood stream, they infect reticulocytes that can be destroyed by phagocytes. Our goal was to assess the importance of monocyte subsets during malaria. We found that P. vivax infection causes an increase in frequency of circulating monocytes, which were defined as classical, inflammatory, and patrolling, based on the expression of membrane molecules. Classical and inflammatory monocytes produced higher levels of pro-inflammatory cytokines and were distinguished from patrolling monocytes by displaying larger and more active mitochondria. Importantly, inflammatory monocytes were more efficient phagocytes; produced high levels of intracellular reactive oxygen species and TNF and consequently control better Plasmodium vivax infection. Hence, our results support the hypothesis that CD14+CD16+ monocytes display effector functions involved in parasite control during malaria.
Zdroje
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