PMID- 23417792
OWN - NLM
STAT- MEDLINE
DCOM- 20140421
LR  - 20211021
IS  - 1573-9368 (Electronic)
IS  - 0962-8819 (Print)
IS  - 0962-8819 (Linking)
VI  - 22
IP  - 5
DP  - 2013 Oct
TI  - Investigation of the kynurenine pathway in Indoleamine 2, 3 dioxygenase deficient 
      mice with inflammatory arthritis.
PG  - 1049-54
LID - 10.1007/s11248-013-9696-5 [doi]
AB  - Tryptophan is an essential amino acid involved in the protein synthesis, 
      cognition, and immunity. Oxidative catabolism of tryptophan is executed by the 
      sets of biochemical reactions collectively referred to as the kynurenine pathway. 
      In the immune system, two distinct enzymes, Indoleamne 2,3 dioxygenase 1 (IDO1) 
      and Indoleamine 2, 3 dioxygenase 2 (IDO2) can initiate metabolic flux through the 
      kynurenine pathway. Rheumatoid arthritis is an autoimmune disease driven by the 
      exacerbated immune response towards self antigens and characterized by the 
      chronic inflammatory reaction of the diarthrodial joints. Collagen induced 
      arthritis (CIA) is an animal model of rheumatoid arthritis. Using CIA in wild 
      type (WT) and mice deficient with Indoleamine 2,3 dioxygenase (Ido1KO), it was of 
      interest to test the impact of Ido1 deletion on the concentration of tryptophan 
      and its catabolites as well as on mRNA expression for other genes on the 
      kynurenine pathway. Here, when compared with samples taken from naive WT animals 
      and those with CIA, it was found that only in the inguinal lymph nodes (iLN) 
      taken from Ido1KO mice with CIA tryptophan concentration was significantly 
      increased. In contrast, mRNA expression for Ido2 was decreased in naive as well 
      as in the diseased iLN taken from Ido1KO mice. Deletion of Ido1 and reduced mRNA 
      expression for Ido2 neither affected the concentration of the downstream 
      metabolites of tryptophan nor mRNA expression for downstream genes on the 
      kynurenine pathway in iLN. Moreover, the concentration of kynurenine in sera of 
      mice with CIA was significantly decreased in Ido1KO mice with arthritis.
FAU - Kolodziej, Lukasz
AU  - Kolodziej L
AD  - The Kennedy Institute of Rheumatology Division, Imperial College London, 
      Arthritis Research UK Building, Charing Cross Hospital Campus, 65 Aspenlea Road, 
      London, W6 8LH, UK, lukasz.kl@interia.pl.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130217
PL  - Netherlands
TA  - Transgenic Res
JT  - Transgenic research
JID - 9209120
RN  - 0 (DNA Primers)
RN  - 0 (IDO1 protein, mouse)
RN  - 0 (IDO2 protein, mouse)
RN  - 0 (Indoleamine-Pyrrole 2,3,-Dioxygenase)
RN  - 343-65-7 (Kynurenine)
RN  - 8DUH1N11BX (Tryptophan)
SB  - IM
MH  - Animals
MH  - Arthritis, Experimental/*metabolism
MH  - Chromatography, High Pressure Liquid
MH  - DNA Primers/genetics
MH  - Indoleamine-Pyrrole 2,3,-Dioxygenase/*deficiency/*metabolism
MH  - Kynurenine/blood/*metabolism
MH  - Lymph Nodes/metabolism
MH  - Metabolic Networks and Pathways/*physiology
MH  - Mice
MH  - Mice, Knockout
MH  - Real-Time Polymerase Chain Reaction
MH  - Tryptophan/*metabolism
PMC - PMC3781305
EDAT- 2013/02/19 06:00
MHDA- 2014/04/22 06:00
PMCR- 2013/02/17
CRDT- 2013/02/19 06:00
PHST- 2012/08/05 00:00 [received]
PHST- 2013/02/04 00:00 [accepted]
PHST- 2013/02/19 06:00 [entrez]
PHST- 2013/02/19 06:00 [pubmed]
PHST- 2014/04/22 06:00 [medline]
PHST- 2013/02/17 00:00 [pmc-release]
AID - 9696 [pii]
AID - 10.1007/s11248-013-9696-5 [doi]
PST - ppublish
SO  - Transgenic Res. 2013 Oct;22(5):1049-54. doi: 10.1007/s11248-013-9696-5. Epub 2013 
      Feb 17.