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Interleukin-10 Regulates Hepcidin in Plasmodium falciparum Malaria
BACKGROUND: Acute malarial anemia remains a major public health problem. Hepcidin, the major hormone controlling the availability of iron, is raised during acute and asymptomatic parasitemia. Understanding the role and mechanism of raised hepcidin and so reduced iron availability during infection is...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3919761/ https://www.ncbi.nlm.nih.gov/pubmed/24520384 http://dx.doi.org/10.1371/journal.pone.0088408 |
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author | Huang, Honglei Lamikanra, Abigail A. Alkaitis, Matthew S. Thézénas, Marie L. Ramaprasad, Abhinay Moussa, Ehab Roberts, David J. Casals-Pascual, Climent |
author_facet | Huang, Honglei Lamikanra, Abigail A. Alkaitis, Matthew S. Thézénas, Marie L. Ramaprasad, Abhinay Moussa, Ehab Roberts, David J. Casals-Pascual, Climent |
author_sort | Huang, Honglei |
collection | PubMed |
description | BACKGROUND: Acute malarial anemia remains a major public health problem. Hepcidin, the major hormone controlling the availability of iron, is raised during acute and asymptomatic parasitemia. Understanding the role and mechanism of raised hepcidin and so reduced iron availability during infection is critical to establish evidence-based guidelines for management of malaria anemia. Our recent clinical evidence suggests a potential role of IL-10 in the regulation of hepcidin in patients with acute P. falciparum malaria. METHODS: We have measured secretion of hepcidin by primary macrophages and the hepatoma cell line HepG2 stimulated with IL-10, IL-6 and Plasmodium falciparum-infected erythrocytes. FINDINGS: We have observed that IL-10 and IL-6 production increased in primary macrophages when these cells were co-cultured with Plasmodium falciparum–infected erythrocytes. We found that IL-10 induced hepcidin secretion in primary macrophages in a dose-dependent manner but not in HepG2 cells. These effects were mediated through signal transducer and activator of transcription (STAT) 3-phosphorylation and completely abrogated by a specific STAT3 inhibitor. CONCLUSION: IL-10 can directly regulate hepcidin in primary macrophages but not in HepG2 cells. This effect can be modulated by Plasmodium falciparum. The results are consistent with a role for IL-10 in modulating iron metabolism during acute phase of infection. |
format | Online Article Text |
id | pubmed-3919761 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-39197612014-02-11 Interleukin-10 Regulates Hepcidin in Plasmodium falciparum Malaria Huang, Honglei Lamikanra, Abigail A. Alkaitis, Matthew S. Thézénas, Marie L. Ramaprasad, Abhinay Moussa, Ehab Roberts, David J. Casals-Pascual, Climent PLoS One Research Article BACKGROUND: Acute malarial anemia remains a major public health problem. Hepcidin, the major hormone controlling the availability of iron, is raised during acute and asymptomatic parasitemia. Understanding the role and mechanism of raised hepcidin and so reduced iron availability during infection is critical to establish evidence-based guidelines for management of malaria anemia. Our recent clinical evidence suggests a potential role of IL-10 in the regulation of hepcidin in patients with acute P. falciparum malaria. METHODS: We have measured secretion of hepcidin by primary macrophages and the hepatoma cell line HepG2 stimulated with IL-10, IL-6 and Plasmodium falciparum-infected erythrocytes. FINDINGS: We have observed that IL-10 and IL-6 production increased in primary macrophages when these cells were co-cultured with Plasmodium falciparum–infected erythrocytes. We found that IL-10 induced hepcidin secretion in primary macrophages in a dose-dependent manner but not in HepG2 cells. These effects were mediated through signal transducer and activator of transcription (STAT) 3-phosphorylation and completely abrogated by a specific STAT3 inhibitor. CONCLUSION: IL-10 can directly regulate hepcidin in primary macrophages but not in HepG2 cells. This effect can be modulated by Plasmodium falciparum. The results are consistent with a role for IL-10 in modulating iron metabolism during acute phase of infection. Public Library of Science 2014-02-10 /pmc/articles/PMC3919761/ /pubmed/24520384 http://dx.doi.org/10.1371/journal.pone.0088408 Text en © 2014 Huang et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Huang, Honglei Lamikanra, Abigail A. Alkaitis, Matthew S. Thézénas, Marie L. Ramaprasad, Abhinay Moussa, Ehab Roberts, David J. Casals-Pascual, Climent Interleukin-10 Regulates Hepcidin in Plasmodium falciparum Malaria |
title | Interleukin-10 Regulates Hepcidin in Plasmodium falciparum Malaria |
title_full | Interleukin-10 Regulates Hepcidin in Plasmodium falciparum Malaria |
title_fullStr | Interleukin-10 Regulates Hepcidin in Plasmodium falciparum Malaria |
title_full_unstemmed | Interleukin-10 Regulates Hepcidin in Plasmodium falciparum Malaria |
title_short | Interleukin-10 Regulates Hepcidin in Plasmodium falciparum Malaria |
title_sort | interleukin-10 regulates hepcidin in plasmodium falciparum malaria |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3919761/ https://www.ncbi.nlm.nih.gov/pubmed/24520384 http://dx.doi.org/10.1371/journal.pone.0088408 |
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