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The role of indoleamine 2,3-dioxygenase in a mouse model of neuroinflammation-induced depression

Nikoletta Dobos, Erik FJ de Vries, Ido P Kema, Konstantinos Patas, Marloes Prins, Ingrid M Nijholt, Rudi Dierckx UGent, Jakob Korf, Johan A den Boer, Paul GM Luiten, et al. (2012) JOURNAL OF ALZHEIMERS DISEASE. 28(4). p.905-915
abstract
Indoleamine 2,3-dioxygenase (IDO), an enzyme which is activated by pro-inflammatory cytokines, has been suggested as a potential link between neuroinflammatory processes in neurodegenerative diseases (like Alzheimer's disease) and depression. The present study aimed to determine whether neuroinflammation-induced increased IDO levels in the mammalian brain will lead to depressive-like behavior. Neuroinflammation was initiated in mice by a single intracerebroventricular injection of lipopolysaccharide (LPS). Cerebral inflammation was monitored 1, 2, 3 and 4 days after the injection with small-animal positron emission tomography (PET) using the inflammatory marker [C-11]-PK11195. In the presence or absence of systemically applied 1-methyl-tryptophan (1-MT), a competitive IDO-inhibitor, we assessed the development of depressive-like behavioral symptoms in parallel with IDO expression and activity. The PK11195 PET signal reached a highly significant peak 3 days after LPS injection, while these animals displayed a significant increase of depressive-like behavior in the forced swim test compared to vehicle-injected animals. These findings were paralleled by a significant increase of IDO in the brainstem, and an increased kynurenine/tryptophan ratio in the serum. Moreover, we report here for the first time, that inhibition of IDO by 1-MT in centrally induced neuroinflammation under experimental conditions can prevent the development of depressive-like behavior.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
neuroinflammation, positron emission tomography, lipopolysaccharide, 3-dioxygenase, indoleamine 2, Depression, ALZHEIMERS-DISEASE, MAJOR DEPRESSION, CALMETTE-GUERIN, 2, 3 DIOXYGENASE, IMMUNE-SYSTEM, RISK-FACTOR, IN-VIVO, BRAIN, LIPOPOLYSACCHARIDE, BEHAVIOR
journal title
JOURNAL OF ALZHEIMERS DISEASE
J. Alzheimers Dis.
volume
28
issue
4
pages
905 - 915
Web of Science type
Article
Web of Science id
000300715600015
JCR category
NEUROSCIENCES
JCR impact factor
4.174 (2012)
JCR rank
64/251 (2012)
JCR quartile
2 (2012)
ISSN
1387-2877
DOI
10.3233/JAD-2011-111097
language
English
UGent publication?
no
classification
A1
id
3151396
handle
http://hdl.handle.net/1854/LU-3151396
date created
2013-02-28 14:53:05
date last changed
2017-05-10 14:19:33
@article{3151396,
  abstract     = {Indoleamine 2,3-dioxygenase (IDO), an enzyme which is activated by pro-inflammatory cytokines, has been suggested as a potential link between neuroinflammatory processes in neurodegenerative diseases (like Alzheimer's disease) and depression. The present study aimed to determine whether neuroinflammation-induced increased IDO levels in the mammalian brain will lead to depressive-like behavior. Neuroinflammation was initiated in mice by a single intracerebroventricular injection of lipopolysaccharide (LPS). Cerebral inflammation was monitored 1, 2, 3 and 4 days after the injection with small-animal positron emission tomography (PET) using the inflammatory marker [C-11]-PK11195. In the presence or absence of systemically applied 1-methyl-tryptophan (1-MT), a competitive IDO-inhibitor, we assessed the development of depressive-like behavioral symptoms in parallel with IDO expression and activity. The PK11195 PET signal reached a highly significant peak 3 days after LPS injection, while these animals displayed a significant increase of depressive-like behavior in the forced swim test compared to vehicle-injected animals. These findings were paralleled by a significant increase of IDO in the brainstem, and an increased kynurenine/tryptophan ratio in the serum. Moreover, we report here for the first time, that inhibition of IDO by 1-MT in centrally induced neuroinflammation under experimental conditions can prevent the development of depressive-like behavior.},
  author       = {Dobos, Nikoletta and de Vries, Erik FJ and Kema, Ido P and Patas, Konstantinos and Prins, Marloes and Nijholt, Ingrid M and Dierckx, Rudi and Korf, Jakob and den Boer, Johan A and Luiten, Paul GM and Eisel, Ulich LM},
  issn         = {1387-2877},
  journal      = {JOURNAL OF ALZHEIMERS DISEASE},
  keyword      = {neuroinflammation,positron emission tomography,lipopolysaccharide,3-dioxygenase,indoleamine 2,Depression,ALZHEIMERS-DISEASE,MAJOR DEPRESSION,CALMETTE-GUERIN,2,3 DIOXYGENASE,IMMUNE-SYSTEM,RISK-FACTOR,IN-VIVO,BRAIN,LIPOPOLYSACCHARIDE,BEHAVIOR},
  language     = {eng},
  number       = {4},
  pages        = {905--915},
  title        = {The role of indoleamine 2,3-dioxygenase in a mouse model of neuroinflammation-induced depression},
  url          = {http://dx.doi.org/10.3233/JAD-2011-111097},
  volume       = {28},
  year         = {2012},
}

Chicago
Dobos, Nikoletta, Erik FJ de Vries, Ido P Kema, Konstantinos Patas, Marloes Prins, Ingrid M Nijholt, Rudi Dierckx, et al. 2012. “The Role of Indoleamine 2,3-dioxygenase in a Mouse Model of Neuroinflammation-induced Depression.” Journal of Alzheimers Disease 28 (4): 905–915.
APA
Dobos, Nikoletta, de Vries, E. F., Kema, I. P., Patas, K., Prins, M., Nijholt, I. M., Dierckx, R., et al. (2012). The role of indoleamine 2,3-dioxygenase in a mouse model of neuroinflammation-induced depression. JOURNAL OF ALZHEIMERS DISEASE, 28(4), 905–915.
Vancouver
1.
Dobos N, de Vries EF, Kema IP, Patas K, Prins M, Nijholt IM, et al. The role of indoleamine 2,3-dioxygenase in a mouse model of neuroinflammation-induced depression. JOURNAL OF ALZHEIMERS DISEASE. 2012;28(4):905–15.
MLA
Dobos, Nikoletta, Erik FJ de Vries, Ido P Kema, et al. “The Role of Indoleamine 2,3-dioxygenase in a Mouse Model of Neuroinflammation-induced Depression.” JOURNAL OF ALZHEIMERS DISEASE 28.4 (2012): 905–915. Print.