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Open AccessJournal ArticleDOI

Absence of kynurenine 3-monooxygenase reduces mortality of acute viral myocarditis in mice

TLDR
It is suggested that increased KP metabolites reduced chemokine production, resulting in suppressed mortality upon KMO knockdown in EMCV infection, and may provide an effective strategy for treating acute viral myocarditis.
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This article is published in Immunology Letters.The article was published on 2017-01-01 and is currently open access. It has received 21 citations till now. The article focuses on the topics: Viral Myocarditis & Kynurenine.

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Journal ArticleDOI

Immune Influencers in Action: Metabolites and Enzymes of the Tryptophan-Kynurenine Metabolic Pathway.

TL;DR: The TRP-KYN pathway is discussed with special emphasis on its interaction with the immune system and the tolerogenic shift towards chronic LGI and overviews the major symptoms, pro- and anti-inflammatory cytokines and toxic and protective KYNs to explore the linkage between chronicLGI, KYNs, and major psychiatric disorders.
Journal Article

Mast Cells Play a Critical Role in the Pathogenesis of Viral Myocarditis : Two Strains of Mast Cell Deficient Mice Study

TL;DR: The role of mast cells in heart failure due to viral myocarditis, using two strains of mast cell-deficient mice, WBB6F1-KitW/KitW-v (W/WV) and WCB6F 1-kitlSl/KitlSl-d (Sl/Sld) was examined in this article.
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Immunomodulatory Effects of Genetic Alterations Affecting the Kynurenine Pathway

TL;DR: This review summarizes experimental data of models in which IDO, TDO, or KMO activity modulation was achieved by interventions affecting enzyme production at a genomic level and indicates that by eliminating or decreasing activities of key enzymes of the kynurenine pathway, a beneficial shift in disease outcome can be attained.
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Lactobacillus johnsonii N6.2 diminishes caspase-1 maturation in the gastrointestinal system of diabetes prone rats.

TL;DR: The role of L. johnsonii in modulating the assembly of the inflammasome as well as some steps of the pro-inflammatory kynurenine pathway is supported.
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Altered kynurenine pathway metabolites in a mouse model of human attention-deficit hyperactivity/autism spectrum disorders: A potential new biological diagnostic marker.

TL;DR: The findings indicate that Ptchd1 KO mice can be used as an animal model of human ADHD and/or ASD, and KP metabolites are potential diagnostic biomarkers for neurodevelopmental disorders.
References
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Journal ArticleDOI

Kynurenines in the mammalian brain: when physiology meets pathology

TL;DR: With recently developed pharmacological agents, it is now possible to restore metabolic equilibrium and envisage novel therapeutic interventions on the basis of the kynurenine pathway.
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Tryptophan-derived Catabolites Are Responsible for Inhibition of T and Natural Killer Cell Proliferation Induced by Indoleamine 2,3-Dioxygenase

TL;DR: It is suggested that IDO exerts its effect on cell proliferation by starting the cascade of biochemical reactions that produce the three catabolites and by enhancing their inhibitory potential by depriving the extracellular microenvironment of tryptophan.
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Inhibition of Allogeneic T Cell Proliferation by Indoleamine 2,3-Dioxygenase–expressing Dendritic Cells Mediation of Suppression by Tryptophan Metabolites

TL;DR: Light is shed on suppressive mechanisms mediated by DCs and an explanation for important biological processes in which IDO activity apparently is increased is provided, such as protection of the fetus from rejection during pregnancy and possibly T cell death in HIV-infected patients.
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Purification and characterization of a novel monocyte chemotactic and activating factor produced by a human myelomonocytic cell line

TL;DR: This represents the first report of the identification and purification of a chemoattractant cytokine that also activates monocytes but is distinct from interferons and other known cytokines.
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Kynurenic Acid as a Ligand for Orphan G Protein-coupled Receptor GPR35

TL;DR: Kynurenic acid stimulates [35S]guanosine 5′-O-(3-thiotriphosphate) binding in GPR35-expressing cells, an effect abolished by pertussis toxin treatment, and inhibits lipopolysaccharide-induced tumor necrosis factor-α secretion in peripheral blood mononuclear cells.
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