A role for interferon-gamma in the hypermetabolic response to murine toxoplasmosis.

Détails

ID Serval
serval:BIB_DD0D884F8584
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
A role for interferon-gamma in the hypermetabolic response to murine toxoplasmosis.
Périodique
European Cytokine Network
Auteur(s)
Arsenijevic D., Bilbao F.D., Giannakopoulos P., Girardier L., Samec S., Richard D.
ISSN
1148-5493 (Print)
ISSN-L
1148-5493
Statut éditorial
Publié
Date de publication
2001
Volume
12
Numéro
3
Pages
518-527
Langue
anglais
Résumé
Toxoplasma gondii (Me49 strain) infection into Swiss Webster mice is followed by hypermetabolism and weight loss in the acute phase lasting 14 days. In the subsequent chronic phase of infection, mice showed either a resolution of hypermetabolism and partial weight recovery (Gainers) or persistent hypermetabolism, with stable weight loss (Non-Gainers). The hypermetabolic response was not associated with an augmentation in the thermogenic uncoupling protein 1 (UCP1) mRNA expression in interscapular brown adipose tissue (BAT), but rather UCP1 expression was reduced. Hypermetabolism is associated with high lipid oxidation as attested by a low respiratory quotient (RQ). Neither BAT nor sympathetic nervous system appear to be involved in the increased lipid utilization, since propranolol did not increase the lower RQ in infected mice. The mitochondrial lipid oxidation blocker mercaptoacetate did not reestablish the respiratory quotient RQ in acute infection (on day 4) and in chronically infected Non-Gainer mice. This suggests an important extra-mitochondrial mechanism of lipid oxidation. Increased lipid peroxidation was detected especially in serum, lung, spleen and liver, which are rich in macrophage-type cells. Following infection peritoneal macrophages exhibited an enhanced capacity to produce reactive oxygen species (ROS). Using IFN-gamma knockout mice we observed that not only the hypermetabolic response was ablated in these mice but there was not a marked increase in ROS production or preferential oxidation/peroxidation of lipids in the acute phase of infection prior to the cachectic phase. The present study described a novel hypermetabolic mechanism involving enhanced lipid peroxidation dependent on IFN-gamma, especially associated with tissues rich in macrophages.
Mots-clé
Adipose Tissue, Brown/metabolism, Animals, Body Weight, Brain/metabolism, Carrier Proteins/metabolism, Cytokines/biosynthesis, Cytokines/blood, Eating/physiology, Energy Metabolism, Interferon-gamma/genetics, Interferon-gamma/metabolism, Ion Channels, Lipid Peroxidation, Macrophages, Peritoneal/metabolism, Male, Membrane Proteins/metabolism, Mice, Mice, Knockout, Mitochondrial Proteins, RNA, Messenger/metabolism, Reactive Oxygen Species/metabolism, Respiration, Spleen/metabolism, Toxoplasma, Toxoplasmosis, Animal/metabolism
Pubmed
Web of science
Création de la notice
14/10/2011 20:04
Dernière modification de la notice
20/08/2019 16:01
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