scholarly journals Indoleamine-2,3-Dioxygenase Mediates Emotional Deficits by the Kynurenine/Tryptophan Pathway in the Ethanol Addiction/Withdrawal Mouse Model

2020 ◽  
Vol 14 ◽  
Author(s):  
Xi Jiang ◽  
Qian Lin ◽  
Lexing Xu ◽  
Ziwei Chen ◽  
Qizhi Yan ◽  
...  
Keyword(s):  
Mouse Model ◽  
Indoleamine 2,3 Dioxygenase ◽  
Tryptophan Pathway ◽  
Emotional Deficits ◽  
Ethanol Addiction

scholarly journals Tryptophan Pathway Abnormalities in a Murine Model of Hereditary Glaucoma

2021 ◽  
Vol 22 (3) ◽  
pp. 1039
Author(s):  
Michal Fiedorowicz ◽  
Tomasz Choragiewicz ◽  
Waldemar A. Turski ◽  
Tomasz Kocki ◽  
Dominika Nowakowska ◽  
...  
Keyword(s):  
Mouse Model ◽  
Murine Model ◽  
Kynurenic Acid ◽  
Pathogenetic Mechanism ◽  
Retinal Tissue ◽  
Indoleamine 2,3 Dioxygenase ◽  
Tryptophan Pathway ◽  
K Concentration ◽  
And Control

Background: It has been shown that a possible pathogenetic mechanism of neurodegeneration in the mouse model of glaucoma (DBA/2J) may be an alteration of kynurenic acid (KYNA) in the retina. This study aimed to verify the hypothesis that alterations of tryptophan (TRP) metabolism in DBA/2J mice is not limited to the retina. Methods: Samples of the retinal tissue and serum were collected from DBA/2J mice (6 and 10 months old) and control C57Bl/6 mice of the same age. The concentration of TRP, KYNA, kynurenine (KYN), and 3-hydroxykynurenine (3OH-K) was measured by HPLC. The activity of indoleamine 2,3-dioxygenase (IDO) was also determined as a KYN/TRP ratio. Results: TRP, KYNA, L-KYN, and 3OH-K concentration were significantly lower in the retinas of DBA/2J mice than in C57Bl/6 mice. 3OH-K concentration was higher in older mice in both strains. Serum TRP, L-KYN, and KYNA concentrations were lower in DBA/2J than in age-matched controls. However, serum IDO activity did not differ significantly between compared groups and strains. Conclusions: Alterations of the TRP pathway seem not to be limited to the retina in the murine model of hereditary glaucoma.

Indoleamine 2,3-dioxygenase–dependent tryptophan metabolites contribute to tolerance induction during allergen immunotherapy in a mouse model

2008 ◽  
Vol 121 (4) ◽  
pp. 983-991.e2 ◽  
Author(s):  
Yousef A. Taher ◽  
Benoit J.A. Piavaux ◽  
Reneé Gras ◽  
Betty C.A.M. van Esch ◽  
Gerard A. Hofman ◽  
...  
Keyword(s):  
Mouse Model ◽  
Allergen Immunotherapy ◽  
Tolerance Induction ◽  
Indoleamine 2,3 Dioxygenase ◽  
Tryptophan Metabolites

scholarly journals 023 Global knockout of immunomodulatory indoleamine 2,3-dioxygenase has no effect on psoriasiform lesions in the imiquimod-induced mouse model of psoriasis

2019 ◽  
Vol 139 (5) ◽  
pp. S4
Author(s):  
V. Choudhary ◽  
E. Ajebo ◽  
R. Uaratanawong ◽  
S. Chowdhury ◽  
S. Hossack ◽  
...  
Keyword(s):  
Mouse Model ◽  
Indoleamine 2,3 Dioxygenase

The therapeutic effect of dendritic cells expressing indoleamine 2,3-dioxygenase (IDO) on an IgA nephropathy mouse model

2020 ◽  
Vol 52 (2) ◽  
pp. 399-407 ◽  
Author(s):  
Kanghan Liu ◽  
Yiya Yang ◽  
Yinyin Chen ◽  
Shiyao Li ◽  
Yuting Gong ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Mouse Model ◽  
Iga Nephropathy ◽  
Therapeutic Effect ◽  
Indoleamine 2,3 Dioxygenase

766: Development and characterization of an indoleamine 2,3-dioxygenase (IDO) deficient mouse model of preeclampsia

2009 ◽  
Vol 201 (6) ◽  
pp. S276
Author(s):  
Mark Santillan ◽  
Christopher Pelham ◽  
Pimonrat Ketsawatsomkron ◽  
Donna Santillan ◽  
Baoli Yang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Deficient Mouse ◽  
Indoleamine 2,3 Dioxygenase

Lipopolysaccharide-induced brain activation of the indoleamine 2,3-dioxygenase and depressive-like behavior are impaired in a mouse model of metabolic syndrome

2014 ◽  
Vol 40 ◽  
pp. 48-59 ◽  
Author(s):  
Anne-Laure Dinel ◽  
Caroline André ◽  
Agnès Aubert ◽  
Guillaume Ferreira ◽  
Sophie Layé ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Mouse Model ◽  
Brain Activation ◽  
Indoleamine 2,3 Dioxygenase

Development of a mouse model of ethanol addiction: naltrexone efficacy in reducing consumption but not craving

2006 ◽  
Vol 113 (9) ◽  
pp. 1305-1321 ◽  
Author(s):  
D. J. Fachin-Scheit ◽  
A. Frozino Ribeiro ◽  
G. Pigatto ◽  
F. Oliveira Goeldner ◽  
R. Boerngen de Lacerda
Keyword(s):  
Mouse Model ◽  
Ethanol Addiction

scholarly journals Iron activates microglia and directly stimulates indoleamine-2,3-dioxygenase activity in the N171-82Q mouse model of Huntington’s disease

2019 ◽  
Author(s):  
David W. Donley ◽  
Marley Realing ◽  
Jason P. Gigley ◽  
Jonathan H. Fox
Keyword(s):  
Mouse Model ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Microglial Activation ◽  
Iron Supplementation ◽  
Kynurenine Pathway ◽  
Indoleamine 2,3 Dioxygenase ◽  
Tryptophan Degradation ◽  
Microglial Morphology

AbstractHuntington’s disease (HD) is a neurodegenerative disorder caused by a dominant CAG-repeat expansion in the huntingtin gene. Morphologic activation of microglia is a key marker of neuroinflammation that is present before clinical onset in HD patients. The kynurenine pathway of tryptophan degradation is restricted in part to microglia and is activated in HD, where it contributes to disease progression. Indoleamine-2,3-dioxygenase (IDO) is a microglial enzyme that catalyzes the first step in this pathway. HD brain microglial cells also accumulate iron; however, the role of iron in promoting microglial activation and the kynurenine pathway is unclear. Based on analyses of morphological characteristics of microglia, we showed that HD mice demonstrate an activated microglial morphology compared with controls. Neonatal iron supplementation resulted in additional microglial morphology changes compared with HD controls. Increased microglial activation in iron-supplemented HD mice was indicated by increased soma volume and decreased process length. In our assessment of whether iron can affect the kynurenine pathway, iron directly enhanced the activity of human recombinant IDO1 with an EC50 of 1.24 nM. We also detected elevated microglial cytoplasmic labile iron in N171-82Q HD mice, an increase that is consistent with the cellular location of IDO. We further demonstrated that neonatal iron supplementation, a model for studying the role of iron in neurodegeneration, activates IDO directly in the mouse brain and promotes neurodegeneration in HD mice. Kynurenine pathway metabolites were also modified in HD and by iron supplementation in wild-type mice. These findings indicate that iron dysregulation contributes to the activation of microglia and the kynurenine pathway in a mouse model of HD.

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