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Clin. Lab. 2014;60:391-396
©Copyright
ORIGINAL ARTICLE
Relation of Kynurenine/Tryptophan with Immune and
Inflammatory Markers in Coronary Artery Disease
YESIM OZKAN
1
, MURAT KADIR SUKUROGLU
2
, MURAT TULMAC
3
,
UCLER KISA
4
, BOLKAN SIMSEK
1
1
Department of Biochemistry, Faculty of Pharmacy, Gazi University, Ankara, Turkey
2
Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Gazi University, Ankara, Turkey
3
Department of Cardiology, School of Medicine, Kırıkkale University, Turkey
4
Department of Biochemistry, School of Medicine, Kırıkkale University, Turkey
SUMMARY
Background: Inflammation and immune activation have a crucial role in the pathogenesis of cardiovascular dis-
eases. Indolamine 2,3-dioxygenase, a tryptophan catabolising enzyme, is up-regulated with various inflammatory
stimuli. The aim of this study was to evaluate the relationship of tryptophan degradation with immune and in-
flammatory markers in coronary artery disease.
Methods: 57 subjects undergoing coronary angiography were recruited. 18 subjects with normal coronary arteries
according to Gensini scoring were selected as a control group and the rest of subjects were included in patient
group. Serum tryptophan and kynurenine levels were determined with HPLC-UV method, and kynurenine/tryp-
tophan ratio was evaluated as IDO activity. Serum neopterin and myeloperoxidase activity were measured by
ELISA method.
Results: While the kynurenine/tryptophan ratio and neopterin levels were similar in both groups, the patient
group had higher myeloperoxidase and hs-CRP levels than controls (p = 0.02, p = 0.002, respectively). The kyn-
urenine/tryptophan ratio was correlated with neopterin in both groups (r = 0.389, p = 0.025; r = 0.683, p = 0.002,
respectively) and with hs-CRP in patients (r = 0.637, p = 0.001). Also, neopterin levels were correlated with hs-
CRP in patients (r = 0.755, p = 0.0001).
Conclusions: Our results are in line with a role of inflammation in coronary artery disease. The study provides
evidence that IDO activity is related with immune and inflammatory states. Also, the study was performed in a
limited hospital-based population. Further studies are warranted in the larger groups.
(Clin. Lab. 2014;60:391-396. DOI: 10.7754/Clin.Lab.2013.121204)
KEY WORDS
atherosclerosis, indolamine 2,3-dioxygenase, kynuren-
ine, neopterin, tryptophan
INTRODUCTION
Atherosclerosis is a primary initiator of coronary artery
diseases, and inflammatory processes are an important
driving force of atherosclerosis and its complications.
For a long time, lipid deposition and smooth muscle cell
proliferation were dominant theories to explain the de-
velopment of atherosclerosis. Nowadays, it has been
established that immune mediated inflammatory mecha-
nisms play a role in this process, and there is more evi-
dence linking initiate and adaptive immune systems to
atherosclerosis [1,2].
Kynurenine (Kyn) is the first stable intermediate formed
from the kynurenine pathway of tryptophan (Trp) deg-
radation. This pathway is initiated either by tryptophan
2,3-dioxygenase (TDO) or indolamine 2,3-dioxygenase
(IDO). Unlike TDO, IDO is widely expressed in most
dendritic cells, macrophages, tumor cells, and endothe-
lial cells and is highly up-regulated locally or systemi-
cally by immune activation and inflammation. This in-
duction is mediated mainly by IFN-Ȗ which is a prion-
flammatory cytokine and a potent stimulant for gene ex-
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Manuscript accepted May 4, 2013