Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/355879
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampCosta, Fabio Trindade Maranhão-
dc.typeArtigopt_BR
dc.titleA first plasmodium vivax natural infection induces increased activity of the interferon gamma-driven tryptophan catabolism pathwaypt_BR
dc.contributor.authorSantos, Rafaella Oliveira dos-
dc.contributor.authorCruz, Maria Geuziane Soares da-
dc.contributor.authorLopes, Stefanie Costa Pinto-
dc.contributor.authorOliveira, Lucas Barbosa-
dc.contributor.authorNogueira, Paulo Afonso-
dc.contributor.authorLima, Emerson Silva-
dc.contributor.authorSoares, Irene Silva-
dc.contributor.authorKano, Flora Satiko-
dc.contributor.authorCarvalho, Andréa Teixeira de-
dc.contributor.authorCosta, Fabio Trindade Maranhão-
dc.contributor.authorGanoza, Christian A.-
dc.contributor.authorLacerda, Marcus Vinicius Guimarães de-
dc.contributor.authorLalwani, Pritesh-
dc.subjectPlasmodium vivaxpt_BR
dc.subject.otherlanguagePlasmodium vivaxpt_BR
dc.description.abstractThe human immune response that controls Plasmodium infection in the liver and blood stages of the parasite life cycle is composed by both pro- and anti-inflammatory programs. Pro-inflammatory responses primarily mediated by IFN-γ controls the infection, but also induce tolerogenic mechanisms to limit host damage, including the tryptophan (TRP) catabolism pathway mediated by the enzyme Indoleamine 2,3-Dioxygenase (IDO1), an enzyme that catalyzes the degradation of TRP to kynurenines (KYN). Here we assessed total serum kynurenines and cytokine dynamics in a cohort of natural Plasmodium vivax human infection and compared them to those of endemic healthy controls and other febrile diseases. In acute malaria, the absolute free kynurenine (KYN) serum levels and the KYN to TRP (KYN/TRP) ratio were significantly elevated in patients compared to healthy controls. Individuals with a diagnosis of a first malaria episode had higher serum KYN levels than individuals with a previous malaria episode. We observed an inverse relationship between the serum levels of IFN-γ and IL-10 in patients with a first malaria episode compared to those of subjects with previous history of malaria. Kynurenine elevation was positively correlated with serum IFN-γ levels in acute infection, whereas, it was negatively correlated with parasite load and P. vivax LDH levels. Overall, the differences observed between infected individuals depended on the number of Plasmodium infections. The decrease in the KYN/TRP ratio in malaria-experienced subjects coincided with the onset of anti-P. vivax IgG. These results suggest that P. vivax infection induces a strong anti-inflammatory program in individuals with first time malaria, which fades with ensuing protective immunity after subsequent episodes. Understanding the tolerance mechanisms involved in the initial exposure would help in defining the balance between protective and pathogenic immune responses necessary to control infection and to improve vaccination strategiespt_BR
dc.relation.ispartofFrontiers in microbiologypt_BR
dc.relation.ispartofabbreviationFront. microbiol.pt_BR
dc.publisher.cityLausannept_BR
dc.publisher.countrySuiçapt_BR
dc.publisherFrontiers Research Foundationpt_BR
dc.date.issued2020-
dc.date.monthofcirculationMar.pt_BR
dc.language.isoengpt_BR
dc.description.volume11pt_BR
dc.description.issuenumber400pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.eissn1664-302Xpt_BR
dc.identifier.doi10.3389/fmicb.2020.00400pt_BR
dc.identifier.urlhttps://www.frontiersin.org/articles/10.3389/fmicb.2020.00400/pt_BR
dc.date.available2021-02-16T11:13:50Z-
dc.date.accessioned2021-02-16T11:13:50Z-
dc.description.provenanceSubmitted by Susilene Barbosa da Silva (susilene@unicamp.br) on 2021-02-16T11:13:50Z No. of bitstreams: 0en
dc.description.provenanceMade available in DSpace on 2021-02-16T11:13:50Z (GMT). No. of bitstreams: 0 Previous issue date: 2020en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/355879-
dc.contributor.departmentDepartamento de Genética, Evolução e Bioagentespt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.subject.keywordTryptophan catabolism pathwaypt_BR
dc.identifier.source000526214900001pt_BR
dc.creator.orcid0000-0001-9969-7300pt_BR
dc.type.formArtigo originalpt_BR
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