Abstract
Infection with Plasmodium vivax results in strong activation of monocytes, which are important components of both the systemic inflammatory response and parasite control. The overall goal of this study was to define the role of monocytes during P. vivax malaria. Here, we demonstrate that P. vivax–infected patients display significant increase in circulating monocytes, which were defined as CD14+CD16− (classical), CD14+CD16+ (inflammatory), and CD14loCD16+ (patrolling) cells. While the classical and inflammatory monocytes were found to be the primary source of pro-inflammatory cytokines, the CD16+ cells, in particular the CD14+CD16+ monocytes, expressed the highest levels of activation markers, which included chemokine receptors and adhesion molecules. Morphologically, CD14+ were distinguished from CD14lo monocytes by displaying larger and more active mitochondria. CD14+CD16+ monocytes were more efficient in phagocytizing P. vivax-infected reticulocytes, which induced them to produce high levels of intracellular TNF-α and reactive oxygen species. Importantly, antibodies specific for ICAM-1, PECAM-1 or LFA-1 efficiently blocked the phagocytosis of infected reticulocytes by monocytes. Hence, our results provide key information on the mechanism by which CD14+CD16+ cells control parasite burden, supporting the hypothesis that they play a role in resistance to P. vivax infection.
Highlights
Plasmodium vivax is the most widely distributed malaria parasite and responsible for approximately 70–80 million cases, annually
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
Summary
Plasmodium vivax is the most widely distributed malaria parasite and responsible for approximately 70–80 million cases, annually. P. vivax is responsible for the majority of malaria cases and represents a significant impediment to social and economic development in Latin America and Asia [1] Both innate and acquired immunity are thought to play critical role in host resistance to infection and pathogenesis of malaria [2,3]. The mechanisms by which the innate immune response mediate resistance to Plasmodium infection or promote a deleterious systemic inflammation associated with malaria sepsis are poorly understood [2]. This is true in the case of P. vivax malaria [4]. The full spectrum of monocyte subsets and the specific functions of each monocyte population during malaria have not been defined
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