dc.creatorSilva, Carlos A. M.
dc.creatorWebb, Kristofor
dc.creatorAndre, Barbara G.
dc.creatorMarques, Maria Angela
dc.creatorCarvalho, Fernanda Marques
dc.creatorMacedo, Cristiana Santos de
dc.creatorPinheiro, Roberta Olmo
dc.creatorSarno, Euzenir Nunes
dc.creatorPessolani, Maria Cristina Vidal
dc.creatorBelisle, John T.
dc.date2018-03-08T12:43:02Z
dc.date2018-03-08T12:43:02Z
dc.date2017
dc.date.accessioned2023-09-26T22:19:41Z
dc.date.available2023-09-26T22:19:41Z
dc.identifierSILVA, Carlos A. M. et al. Type 1 Reaction in Patients With Leprosy Corresponds to a Decrease in Proresolving Lipid Mediators and an Increase in Proinflammatory Lipid Mediators. The Journal of Infectious Diseases, v. 215, p. 431-439, Feb. 2017.
dc.identifier0022-1899
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/25185
dc.identifier10.1093/infdis/jiw541
dc.identifier1537-6613
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8877901
dc.descriptionBackground. Type 1 reaction (T1R) is an acute T-helper type 1 (Th1) inflammatory episode in patients with leprosy. While immunological responses associated with T1R have been investigated, the corresponding metabolic responses that could contribute to T1R pathology have received little attention. Methods. Metabolomics-based analyses of sera from 7 patients with and 9 without T1R were conducted via liquid chromatography–mass spectrometry. Serum metabolites present at levels that significantly differed (P < .05) with a log2 fold change of ≥ 1.0 between patient groups were interrogated against known metabolic pathways. The structural identification of targeted metabolites was confirmed and abundance changes validated by mass spectrometry and enzyme-linked immunoassay. Results. Forty metabolic pathways were perturbed in patients with T1R, with 71 dysregulated metabolites mapping to pathways for lipid mediators of inflammation. Of note was an increase in the abundance of the proinflammatory leukotriene B4 (LTB4) and a corresponding decrease in the level of proresolving resolvin D1 (RvD1). Also, levels of prostaglandin D2 (PGD2) and lipoxin A4 (LXA4) in patients with T1R were significantly increased, while the level of prostaglandin E2 (PGE2) was decreased. Conclusions. The dysregulation of metabolic pathways leading to abundance shifts between proinflammatory and proresolving lipid mediators provides a link between metabolic and cellular immune responses that result in the Th1-mediated pathology of T1R.
dc.description2030-01-01
dc.formatapplication/pdf
dc.languageeng
dc.publisherOxford University Press
dc.rightsrestricted access
dc.subjectHanseníase
dc.subjectReação tipo 1
dc.subjectMetabolômica
dc.subjectmediadores de prorestação especializados
dc.subjectMediadores lipídicos pró-inflamatórios
dc.subjectLeprosy
dc.subjecttype 1 reaction
dc.subjectmetabolomics
dc.subjectlipid mediators
dc.subjectspecialized proresolving mediators
dc.titleType 1 Reaction in Patients With Leprosy Corresponds to a Decrease in Proresolving Lipid Mediators and an Increase in Proinflammatory Lipid Mediators
dc.typeArticle


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