Vaccines R&D & Vaccination

Dietmar Fuchs has completed his PhD (Chemistry) from Innsbruck University. He is the Deputy Director of the Division of Biological Chemistry at Innsbruck Medical University and from 1997-2006, he was Co-director of the Ludwig Boltzmann Institute for AIDS-Research in Innsbruck. He has published more than 500 scientific articles in the fields of clinical immunology, immunobiology, neuroimmunology, biochemistry and chemistry of pteridines, indoleamine 2, 3-dioxygenase (IDO) homocysteine, and oxidative stress in reputed journals and has been serving as an Editorial Board Member of repute. He is Honorary Member of the Austrian Society of Laboratory Medicine and Clinical Chemistry (2011).

Within the so-called Th1-type immune response, the pro-inflammatory cytokine interferon-g (IFN-g) accelerates the effectiveness of immunity. IFN-g coordinates T-cell activation and induces several anti-proliferative pathways aimed to halt the growth of pathogens and of malignant cells. Among these pathways, the induction of pteridine-forming enzyme GTP-cyclohydrolase 1 of the tryptophan-degrading enzyme indoleamine 2, 3-dioxygenase-1 and the production of reactive oxygen species (ROS) play important roles. Accordingly, increasing concentrations of the pteridine neopterin and of tryptophan breakdown as expressed by the kynurenine to tryptophan ratio (Kyn/Trp), parallel the course of chronic inflammatory disease. A long-term discussion is whether administration of antioxidants would reduce ROS damage and represent a preventive and potentially therapeutic strategy to combat inflammatory diseases. In human peripheral blood mononuclear cells, IFN-g and neopterin formation and cytokine-induced tryptophan breakdown are suppressed dose-dependently upon addition of antioxidative compounds like vitamin C and E. Food preservatives, colorants and supplements such as sodium sulfite and benzoate, curcumin and beet root juice act in a similar manner. The antioxidant nature of these products can interfere with pro-inflammatory cytokine cascades and interrupt immunologic pathways, which enforce the development and progression of several inflammatory disorders such as cardiovascular or neurodegenerative diseases. However, due to the cross-regulation of Th1- and Th2-type immunity, any specific suppression of Th1-type immune response bears the risk of up-regulating counter-regulatory mechanisms of Th2-type immunity. Thus, a potential side effect of the wide-spread use of antioxidant food additives could be an increased frequency of allergic responses due to the suppression of Th1-type immunity. However, more in vivo studies are still required to further substantiate the validity of these considerations.