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2030-01-01
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TYPE 1 REACTION IN PATIENTS WITH LEPROSY CORRESPONDS TO A DECREASE IN PRORESOLVING LIPID MEDIATORS AND AN INCREASE IN PROINFLAMMATORY LIPID MEDIATORS
Silva, Carlos A. M. et al. | Date Issued: 2017
Author
Silva, Carlos A. M.
Webb, Kristofor
Andre, Barbara G.
Marques, Maria Angela
Carvalho, Fernanda Marques
Macedo, Cristiana Santos de
Pinheiro, Roberta Olmo
Sarno, Euzenir Nunes
Pessolani, Maria Cristina Vidal
Belisle, John T.
Affilliation
Colorado State University. Mycobacteria Research Laboratories. Fort Collins, Co, USA / Colorado State University. Department of Microbiology, Immunology, and Pathology. Fort Collins, CO, USA.
Colorado State University. Mycobacteria Research Laboratories. Fort Collins, Co, USA / Colorado State University. Department of Microbiology, Immunology, and Pathology. Fort Collins, CO, USA.
Colorado State University. Department of Microbiology, Immunology, and Pathology. Fort Collins, CO, USA.
Colorado State University. Mycobacteria Research Laboratories. Fort Collins, Co, USA / Colorado State University. Department of Microbiology, Immunology, and Pathology. Fort Collins, CO, USA. / Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Microbiologia Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Microbiologia Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Microbiologia Celular. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz. Centro de Desenvolvimento Tecnológico em Saúde. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ. Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ. Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Microbiologia Celular. Rio de Janeiro, RJ, Brasil.
Colorado State University. Mycobacteria Research Laboratories. Fort Collins, Co, USA / Colorado State University. Department of Microbiology, Immunology, and Pathology. Fort Collins, CO, USA.
Abstract
Background. 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.
Keywords in Portuguese
Hanseníase
Reação tipo 1
Metabolômica
mediadores de prorestação especializados
Mediadores lipídicos pró-inflamatórios
 
Keywords
Leprosy
type 1 reaction
metabolomics
lipid mediators
specialized proresolving mediators
 
Publisher
Oxford University Press
Citation
SILVA, 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.
DOI
10.1093/infdis/jiw541
ISSN
0022-1899