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https://www.arca.fiocruz.br/handle/icict/9844
THE CD14+CD16+ INFLAMMATORY MONOCYTE SUBSET DISPLAYS INCREASED MITOCHONDRIAL ACTIVITY AND EFFECTOR FUNCTION DURING ACUTE PLASMODIUM VIVAX MALARIA
Author
Affilliation
Fundacao Oswaldo Cruz. Centro de Pesquisas Rene Rachou. Laboratorio de Immunopatologia. Belo Horizonte, MG, Brazil
Fundacao Oswaldo Cruz. Centro de Pesquisas Rene Rachou. Laboratorio de Immunopatologia. Belo Horizonte, MG, Brazil
Fundacao Oswaldo Cruz. Centro de Pesquisas Rene Rachou. Laboratorio de Immunopatologia. Belo Horizonte, MG, Brazil
Fundacao Oswaldo Cruz. Centro de Pesquisas Rene Rachou. Laboratorio de Immunopatologia. Belo Horizonte, MG, Brazil/Universidade Federal de Minas Gerais. Departamento de Bioquımica e Imunologia. Belo Horizonte, MG, Brazil
Centro de Pesquisas em Medicina Tropical de Rondonia. Porto Velho, RO, Brazil
Centro de Pesquisas em Medicina Tropical de Rondonia. Porto Velho, RO, Brazil
Fundacao Oswaldo Cruz. Centro de Pesquisas Rene Rachou. Laboratorio de Biomarcadores de Diagnostico e Monitoracao. Belo Horizonte, MG, Brazil
University of Massachusetts Medical School. Division of Infectious Diseases and Immunology. Worcester, MA, United States of America
Universidade Federal de Minas Gerais. Departamento de Patologia Geral. Belo Horizonte, MG, Brazil
Fundacao Oswaldo Cruz. Centro de Pesquisas Rene Rachou. Laboratorio de Immunopatologia. Belo Horizonte, MG, Brazil/Universidade Federal de Minas Gerais. Departamento de Bioquımica e Imunologia. Belo Horizonte, MG, Brazil
Fundacao Oswaldo Cruz. Centro de Pesquisas Rene Rachou. Laboratorio de Immunopatologia. Belo Horizonte, MG, Brazil
Fundacao Oswaldo Cruz. Centro de Pesquisas Rene Rachou. Laboratorio de Immunopatologia. Belo Horizonte, MG, Brazil
Fundacao Oswaldo Cruz. Centro de Pesquisas Rene Rachou. Laboratorio de Immunopatologia. Belo Horizonte, MG, Brazil/Universidade Federal de Minas Gerais. Departamento de Bioquımica e Imunologia. Belo Horizonte, MG, Brazil
Centro de Pesquisas em Medicina Tropical de Rondonia. Porto Velho, RO, Brazil
Centro de Pesquisas em Medicina Tropical de Rondonia. Porto Velho, RO, Brazil
Fundacao Oswaldo Cruz. Centro de Pesquisas Rene Rachou. Laboratorio de Biomarcadores de Diagnostico e Monitoracao. Belo Horizonte, MG, Brazil
University of Massachusetts Medical School. Division of Infectious Diseases and Immunology. Worcester, MA, United States of America
Universidade Federal de Minas Gerais. Departamento de Patologia Geral. Belo Horizonte, MG, Brazil
Fundacao Oswaldo Cruz. Centro de Pesquisas Rene Rachou. Laboratorio de Immunopatologia. Belo Horizonte, MG, Brazil/Universidade Federal de Minas Gerais. Departamento de Bioquımica e Imunologia. Belo Horizonte, MG, Brazil
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+CD162 (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. vivaxinfected reticulocytes, which induced them to produce high levels of intracellular TNF-a 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.
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