Interleukin-10 regulates hepcidin in Plasmodium falciparum malaria

Handle URI:
http://hdl.handle.net/10754/325334
Title:
Interleukin-10 regulates hepcidin in Plasmodium falciparum malaria
Authors:
Huang, Honglei; Lamikanra, Abigail A.; Alkaitis, Matthew S.; Thézénas, Marie L.; Ramaprasad, Abhinay ( 0000-0001-9372-5526 ) ; Moussa, Ehab; Roberts, David J.; Casals-Pascual, Climent
Abstract:
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. 2014 Huang et al.
Citation:
Huang H, Lamikanra AA, Alkaitis MS, Thézénas ML, Ramaprasad A, et al. (2014) Interleukin-10 Regulates Hepcidin in Plasmodium falciparum Malaria. PLoS ONE 9: e88408. doi:10.1371/journal.pone.0088408.
Publisher:
Public Library of Science (PLoS)
Journal:
PLoS ONE
Issue Date:
10-Feb-2014
DOI:
10.1371/journal.pone.0088408
PubMed ID:
24520384
PubMed Central ID:
PMC3919761
Type:
Article
ISSN:
19326203
Appears in Collections:
Articles

Full metadata record

DC FieldValue Language
dc.contributor.authorHuang, Hongleien
dc.contributor.authorLamikanra, Abigail A.en
dc.contributor.authorAlkaitis, Matthew S.en
dc.contributor.authorThézénas, Marie L.en
dc.contributor.authorRamaprasad, Abhinayen
dc.contributor.authorMoussa, Ehaben
dc.contributor.authorRoberts, David J.en
dc.contributor.authorCasals-Pascual, Climenten
dc.date.accessioned2014-08-27T09:47:33Zen
dc.date.available2014-08-27T09:47:33Zen
dc.date.issued2014-02-10en
dc.identifier.citationHuang H, Lamikanra AA, Alkaitis MS, Thézénas ML, Ramaprasad A, et al. (2014) Interleukin-10 Regulates Hepcidin in Plasmodium falciparum Malaria. PLoS ONE 9: e88408. doi:10.1371/journal.pone.0088408.en
dc.identifier.issn19326203en
dc.identifier.pmid24520384en
dc.identifier.doi10.1371/journal.pone.0088408en
dc.identifier.urihttp://hdl.handle.net/10754/325334en
dc.description.abstractBackground: 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. 2014 Huang et al.en
dc.language.isoenen
dc.publisherPublic Library of Science (PLoS)en
dc.rightsThis is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en
dc.subjecthepcidinen
dc.subjectinterleukin 10en
dc.subjectinterleukin 6en
dc.subjectSTAT3 proteinen
dc.subjectcell specificityen
dc.subjectcell stimulationen
dc.subjectcell strain HepG2en
dc.subjectcocultureen
dc.subjectconcentration responseen
dc.subjectcontrolled studyen
dc.subjectcytokine productionen
dc.subjectdisease courseen
dc.subjecterythrocyteen
dc.subjecthormonal regulationen
dc.subjecthormone releaseen
dc.subjecthost parasite interactionen
dc.subjecthuman cellen
dc.subjectin vitro studyen
dc.subjectiron metabolismen
dc.subjectmacrophageen
dc.subjectmalaria falciparumen
dc.subjectpathophysiologyen
dc.subjectPlasmodium falciparumen
dc.subjectprotein analysisen
dc.subjectprotein functionen
dc.subjectprotein phosphorylationen
dc.subjectregulatory mechanismen
dc.titleInterleukin-10 regulates hepcidin in Plasmodium falciparum malariaen
dc.typeArticleen
dc.identifier.journalPLoS ONEen
dc.identifier.pmcidPMC3919761en
dc.eprint.versionPublisher's Version/PDFen
dc.contributor.institutionWellcome Trust Centre for Human Genetics, Oxford, United Kingdomen
dc.contributor.institutionNuffield Department of Clinical Laboratory Sciences, University of Oxford, John Radcliffe Hospital, Headington, Oxford, United Kingdomen
dc.contributor.institutionLaboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, Rockville, MD, United Statesen
dc.contributor.affiliationKing Abdullah University of Science and Technology (KAUST)en
kaust.authorRamaprasad, Abhinayen
kaust.authorMoussa, Ehaben

Related articles on PubMed

All Items in KAUST are protected by copyright, with all rights reserved, unless otherwise indicated.