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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/61018
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dc.creatorBijay Bajracharyapt_BR
dc.creatorDeena Shresthapt_BR
dc.creatorAndre Talvani Pedrosa da Silvapt_BR
dc.creatorRicardo Gonçalvespt_BR
dc.creatorLuis Carlos Crocco Afonsopt_BR
dc.date.accessioned2023-11-16T21:22:44Z-
dc.date.available2023-11-16T21:22:44Z-
dc.date.issued2022-02-11-
dc.citation.volume2022pt_BR
dc.citation.spage9928362pt_BR
dc.citation.epage10pt_BR
dc.identifier.doihttps://doi.org/10.1155/2022/9928362pt_BR
dc.identifier.issn2314-6141pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/61018-
dc.description.resumoEndogenous nucleotides produced by various group of cells under inflammatory conditions act as potential danger signals in vivo. Extracellularly released nucleotides such as ATP are rapidly hydrolyzed to adenosine by the coordinated ectonucleotidase activities of CD39 and CD73. Leishmania is an obligate intracellular parasite of macrophages and capable of modulating host immune response in order to survive and multiply within host cells. In this study, the activity of CD73 induced by Leishmania amazonensis in infected macrophages has been investigated and correlated with parasite survival and infection in vitro. For this, the expression of CD39 and CD73, by flow cytometry, in murine peritoneal macrophages infected with metacyclic promastigotes of L. amazonensis has been analyzed. Our results showed that L. amazonensis-infected macrophages, unlike LPS-treated macrophages, increased CD73 expression. It was also noted that when CD73 enzymatic activity was blocked by α, β-methyleneadenosine 5-diphosphate sodium salt (APCP), macrophage parasitism was significantly decreased. Interestingly, these effects were not associated with the production of TNF-α, IL-10, or nitric oxide (NO). Together, these data demonstrate that L. amazonensis induces a regulatory phenotype in macrophages, which by activating the CD39/CD73 pathway allows parasite survival through the action of immunomodulatory adenosine receptors.pt_BR
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológicopt_BR
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Geraispt_BR
dc.description.sponsorshipCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superiorpt_BR
dc.format.mimetypepdfpt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE PATOLOGIApt_BR
dc.publisher.departmentICB - INSTITUTO DE CIÊNCIAS BIOLOGICASpt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofBioMed Research Internationalpt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectLeishmaniapt_BR
dc.subjectInflammationpt_BR
dc.subjectMacrophagespt_BR
dc.subjectEctonucleotidasespt_BR
dc.subject.otherMacrófagospt_BR
dc.subject.otherInflamaçãopt_BR
dc.subject.otherLeishmaniapt_BR
dc.titleThe Ecto-5′nucleotidase/CD73 Mediates Leishmania amazonensis Survival in Macrophagespt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.hindawi.com/journals/bmri/2022/9928362/pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-2476-821Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-1281-5330pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-6685-6229pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-1127-4483pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-2498-4086pt_BR
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