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J Am Coll Cardiol, 2004; 43:1132, doi:10.1016/j.jacc.2003.12.029 © 2004 by the American College of Cardiology Foundation |
Institute of Medical Chemistry and Biochemistry, Department of Psychiatry, University of Innsbruck, Ludwig Boltzmann Institute of AIDS Research, Fritz Pregl Strasse 3, A-6020 Innsbruck, Austria
dietmar.fuchs{at}uibk.ac.at
) and interleukins (IL)-2 and -12, while promoting secretion of Th-2 cytokines IL-4, IL-5, and IL-10 (2). Such data favorably compare to results we have generated in vitro on atorvastatin to suppress IFN-
-mediated biochemical events in peripheral blood mononuclear cells and in monocytes (3). Atorvastatin was shown to diminish in a dose-dependent manner activity of indoleamine (2,3)-dioxygenase (IDO). Enzyme IDO is inducible by IFN-
and degrades the essential amino acid tryptophan via the kynurenine pathway. Therefore, accelerated tryptophan degradation by IDO activation is commonly observed in a broad range of diseases associated with endogenous formation of Th1-type cytokine IFN-
(4), including patients with coronary heart disease (CHD) (5). Because tryptophan is precursor of neurotransmitter 5-hydroxytryptamine (serotonin), lowered tryptophan availability increases the susceptibility of depression in patients (4); for example, in patients with colorectal cancer an association was reported between lowered serum tryptophan related to immune activation and impaired quality of life (6). Thus, when statins are able to block IDO and thereby increase tryptophan concentrations, it is reasonable that statins would reduce the risk of depression in CHD patients with an accelerated tryptophan degradation (5). Whether statins improve tryptophan metabolism in patients is worth being tested in clinical trials.
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-induced neopterin formation and tryptophan degradation in human peripheral blood mononuclear cells and in monocytic cell lines. Clin Exp Immunol. 2003;131:264267[CrossRef][Medline]
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