Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/342321
Type: Artigo
Title: Kynurenine elevation correlates with T regulatory cells increase in acute plasmodium vivax infection : a pilot study
Author: dos Santos, Rafaella Oliveira
Goncalves-Lopes, Raquel M.
Lima, Nathalia F.
Scopel, Kezia K. G.
Ferreira, Marcelo U.
Lalwani, Pritesh
Abstract: Disease-tolerance mechanisms limit infection severity by preventing tissue damage; however, the underlying mechanisms in human malaria are still unclear. Tryptophan (TRP), an essential amino acid, is catabolized into tolerogenic metabolites, kynurenines (KYN), by indoleamine 2,3-dioxygenase 1 (IDO1), which can induce Foxp3+ T regulatory cells (Tregs). In this study, we evaluated the relationship of these metabolites with Treg-mediated tolerance induction in acute malaria infections. We performed a cross-sectional study that evaluated asymptomatic, symptomatic malaria patients and endemic control patient groups. We assessed plasmatic concentration of cytokines by ELISA. Plasmatic TRP and KYN levels were measured by HPLC. Peripheral T regulatory cells were measured and phenotyped by flow cytometry. The KYN/TRP ratio was significantly elevated in asymptomatic and symptomatic Plasmodium infection, compared to healthy controls. Also, Th1 and Th2 cytokines were elevated in the acute phase of malaria disease. IFN-gamma increase in acute phase was positively correlated with the KYN/TRP ratio and KYN elevation was positively correlated with the increase of peripheral FoxP3+ T regulatory cells. Additional studies are needed not only to identify innate mechanisms that increase tryptophan catabolism but also the role of Tregs in controlling malaria-induced pathology and malaria tolerance by the host
Subject: Inflamação
Country: Reino Unido
Editor: Wiley
Rights: Fechado
Identifier DOI: 10.1111/pim.12689
Address: https://onlinelibrary.wiley.com/doi/full/10.1111/pim.12689
Date Issue: 2020
Appears in Collections:HEMO - Artigos e Outros Documentos

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