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Bone marrow chimeric mice reveal a dual role for CD36 in Plasmodium berghei ANKA infection

2007-03-16Artigo científico Acesso aberto
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dc.contributor.authorCunha Rodrigues, Margarida
dc.contributor.authorPortugal, Silvia
dc.contributor.authorFebbraio, Maria
dc.contributor.authorMota, Maria M.
dc.date.accessioned2021-05-14T11:35:40Z
dc.date.available2021-05-14T11:35:40Z
dc.date.issued2007-03-16
dc.description© 2007 Cunha-Rodrigues et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.pt_PT
dc.description.abstractBackground: Adhesion of Plasmodium-infected red blood cells (iRBC) to different host cells, ranging from endothelial to red blood cells, is associated to malaria pathology. In vitro studies have shown the relevance of CD36 for adhesion phenotypes of Plasmodium falciparum iRBC such as sequestration, platelet mediated clumping and non-opsonic uptake of iRBC. Different adhesion phenotypes involve different host cells and are associated with different pathological outcomes of disease. Studies with different human populations with CD36 polymorphisms failed to attribute a clear role to CD36 expression in human malaria. Up to the present, no in vivo model has been available to study the relevance of different CD36 adhesion phenotypes to the pathological course of Plasmodium infection. Methods: Using CD36-deficient mice and their control littermates, CD36 bone marrow chimeric mice, expressing CD36 exclusively in haematopoietic cells or in non-haematopoietic cells, were generated. Irradiated CD36-/- and wild type mice were also reconstituted with syngeneic cells to control for the effects of irradiation. The reconstituted mice were infected with Plasmodium berghei ANKA and analysed for the development of blood parasitaemia and neurological symptoms. Results: All mice reconstituted with syngeneic bone marrow cells as well as chimeric mice expressing CD36 exclusively in non-haematopoietic cells died from experimental cerebral malaria between day 6 and 12 after infection. A significant proportion of chimeric mice expressing CD36 only in haematopoietic cells did not die from cerebral malaria. Conclusion: The analysis of bone marrow chimeric mice reveals a dual role of CD36 in P. berghei ANKA infection. Expression of CD36 in haematopoietic cells, most likely macrophages and dendritic cells, has a beneficial effect that is masked in normal mice by adverse effects of CD36 expression in non-haematopoietic cells, most likely endothelial cells.pt_PT
dc.description.sponsorshipThis work was supported by Fundação para a Ciência e Tecnologia grant POCI/BIA-BCM/61799/2004 to MMM. MCR and SP are supported by FCT Fellowships, SFRH/BD/8435/2002 and SFRH/BD/31523/2006 respectively. MMM is a Fellow of the EMBO YIP and is a Howard Hughes Medical Institute International Research Scholar.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationMalar J. 2007 Mar 16;6:32pt_PT
dc.identifier.doi10.1186/1475-2875-6-32pt_PT
dc.identifier.eissn1475-2875
dc.identifier.urihttp://hdl.handle.net/10451/47856
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherSpringer Naturept_PT
dc.relationThe role of Plasmodium molecules that migrate to the host cell nucleus during the hepatocyte infection
dc.relationSIGNALLING PATHWAYS REQUIRED FOR PLASMODIUM LIVER INFECTION
dc.relation.publisherversionhttps://malariajournal.biomedcentral.com/pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.titleBone marrow chimeric mice reveal a dual role for CD36 in Plasmodium berghei ANKA infectionpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardNumberPOCI/BIA-BCM/61799/2004
oaire.awardNumberSFRH/BD/8435/2002
oaire.awardNumberSFRH/BD/31523/2006
oaire.awardTitleThe role of Plasmodium molecules that migrate to the host cell nucleus during the hepatocyte infection
oaire.awardTitleSIGNALLING PATHWAYS REQUIRED FOR PLASMODIUM LIVER INFECTION
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/POCI/POCI%2FBIA-BCM%2F61799%2F2004/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBD%2F8435%2F2002/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F31523%2F2006/PT
oaire.citation.titleMalaria Journalpt_PT
oaire.citation.volume6pt_PT
oaire.fundingStreamPOCI
oaire.fundingStreamSFRH
person.familyNamePortugal
person.familyNameMota
person.givenNameSilvia
person.givenNameMaria Manuel
person.identifier.ciencia-idF91F-0A41-F2FD
person.identifier.ciencia-id4217-0969-297E
person.identifier.orcid0000-0003-4567-9101
person.identifier.orcid0000-0002-2858-1041
person.identifier.scopus-author-id7102709816
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
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