TY  - JOUR
A1  - Garcia, Ada
A1  - Rühl, Ralph
A1  - Herz, U.
A1  - Koebnick, Corinna
A1  - Schweigert, Florian J.
A1  - Worm, Margitta
T1  - Retinoid- and carotenoid-enriched diets influence the ontogenesis of the immune system in mice
Y1  - 2003
ER  - 
TY  - JOUR
A1  - Koch, Christin
A1  - Brovkina, Lioudmila
A1  - Rühl, Ralph
A1  - Worm, Margitta
T1  - Immunomodulation by dietary n3-polyunsaturated fatty acids (PUFA) in vitro
Y1  - 2006
SN  - 0091-6749
ER  - 
TY  - JOUR
A1  - Rühl, Ralph
A1  - Garcia, Ada
A1  - Schweigert, Florian J.
A1  - Worm, Margitta
T1  - Modulation of cytokine production by low and high retinoid diet in ovalbumin-sensitized mice
N2  - Retinoids modulate many physiological processes such as the differentiation and growth of different cell types. including cells from the immune system. We have previously shown that retinoids modulate IgE production in vitro and in vivo. In the present study we investigated the effects of retinoids in non-sensitized and ovalbumin-sensitized mice that were fed for 11 weeks with three different vitamin A (VA) diets: a) VA-deficiency diet, b) base diet, and c) base diet supplemented with 0.5% all-trans-retinoic acid (ATRA). Phorbol-myristate-acetate (PMA)/ionomycin-stimulated SMC (splenic mononuclear cells) from mice fed with ATRA and the vitamin A-deficient diet group showed increased interleukin-4 (IL-4) responses in non-sensitized mice. After ovalbumin sensitization in the VA-deficient and the ATRA supplementation diet groups, no significant effects on IL-4 production were observed. By contrast, gamma interferon (IFN-gamma production from PMA/ionomycin-stimulated SMC was enhanced in the VA-deficient diet group in ovalbumin-sensitized mice, and also in non-sensitized mice compared to the base and the ATRA-supplemented diet group. The data indicate that VA and retinoid content in a diet influences the cytokine response in non-sensitized and also ovalbumin-sensitized mice. Therefore these molecules may serve as active modulators of cytokine production in vivo that are responsible for the induction and persistence of atopic diseases
Y1  - 2004
ER  -