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Indoleamine 2,3-dioxygenase 1 is upregulated in activated microglia in mice cerebellum during acute viral encephalitis.

Authors :
Taguchi A
Niwa M
Hoshi M
Saito K
Masutani T
Hisamatsu K
Kobayashi K
Hatano Y
Tomita H
Hara A
Source :
Neuroscience letters [Neurosci Lett] 2014 Apr 03; Vol. 564, pp. 120-5. Date of Electronic Publication: 2014 Feb 12.
Publication Year :
2014

Abstract

Indoleamine 2,3-dioxygenase1 (IDO1) is the rate-limiting enzyme in the kynurenine pathway that converts l-tryptophan to l-kynurenine. Encephalomyocarditis virus (EMCV) can cause acute myocarditis in various animals including mice. Previously, IDO1 has been reported to have an important immunomodulatory function in immune-related diseases. However, the pathophysiological roles of IDO1 following acute viral infection of central nervous system are not fully understood. We observed that acute EMCV infection leads to a highly reproducible neuronal degeneration in mouse cerebellum. The goal of this study is to determine tissue/cell-specific and time-dependent expressions of IDO1 during acute EMCV infection in mouse cerebellum. IDO1 was up-regulated in microglia, which was recognized to be activated morphologically and positive for ionized calcium-binding adapter molecule 1 (Iba-1), a protein expressed in microglia, within EMCV-induced cerebellar lesions showing neuronal degeneration although the very weak expression of IDO1 is detected only in cytoplasm of Purkinje cells. No GFAP immunostaining was observed in EMCV-induced cerebellar lesions although many reactive astrocytes surrounding the lesions showed strongly positive immunostaining for GFAP 10 days after the viral inoculation. Thus, IDO1 expression may affect EMCV-induced neuronal degeneration in cerebellum.<br /> (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Details

Language :
English
ISSN :
1872-7972
Volume :
564
Database :
MEDLINE
Journal :
Neuroscience letters
Publication Type :
Academic Journal
Accession number :
24530381
Full Text :
https://doi.org/10.1016/j.neulet.2014.01.051