Serveur d'exploration sur les relations entre la France et l'Australie

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Characterization of the Kynurenine Pathway and Quinolinic Acid Production in Macaque Macrophages

Identifieur interne : 004796 ( Main/Exploration ); précédent : 004795; suivant : 004797

Characterization of the Kynurenine Pathway and Quinolinic Acid Production in Macaque Macrophages

Auteurs : Chai K. Lim [Australie] ; Margaret M. C. Yap [Australie] ; Stephen J. Kent [Australie] ; Gabriel Gras [France] ; Boubekeur Samah [France] ; Jane C. Batten [Australie] ; Robert De Rose [Australie] ; Benjamin Heng [Australie] ; Bruce J. Brew [Australie] ; Gilles J. Guillemin [Australie]

Source :

RBID : PMC:3662399

Abstract

The kynurenine pathway (KP) and one of its end-products, the excitotoxin quinolinic acid (QUIN), are involved in the pathogenesis of several major neuroinflammatory brain diseases. A relevant animal model to study KP metabolism is now needed to assess whether intervention in this pathway may improve the outcome of such diseases. Humans and macaques share a very similar genetic makeup. In this study, we characterized the KP metabolism in macaque primary macrophages of three different species in comparison to human cells. We found that the KP profiles in simian macrophages were very similar to those in humans when challenged with inflammatory cytokines. Further, we found that macaque macrophages are capable of producing a pathophysiological concentration of QUIN. Our data validate the simian model as a relevant model to study the human cellular KP metabolism in the context of inflammation.


Url:
DOI: 10.4137/IJTR.S11789
PubMed: 23761975
PubMed Central: 3662399


Affiliations:


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Le document en format XML

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<p>The kynurenine pathway (KP) and one of its end-products, the excitotoxin quinolinic acid (QUIN), are involved in the pathogenesis of several major neuroinflammatory brain diseases. A relevant animal model to study KP metabolism is now needed to assess whether intervention in this pathway may improve the outcome of such diseases. Humans and macaques share a very similar genetic makeup. In this study, we characterized the KP metabolism in macaque primary macrophages of three different species in comparison to human cells. We found that the KP profiles in simian macrophages were very similar to those in humans when challenged with inflammatory cytokines. Further, we found that macaque macrophages are capable of producing a pathophysiological concentration of QUIN. Our data validate the simian model as a relevant model to study the human cellular KP metabolism in the context of inflammation.</p>
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