Immune enhancement activities of silk lutein extract from Bombyx mori cocoons.

BACKGROUND: Declining immune function poses an important clinical challenge worldwide and supplementation with natural products that possessing immune enhancing properties is a promising approach for preventing or delaying immune function decline. Cocoons from yellow silkworms are a significant source of lutein, and this unexplored silk extract could be a viable alternative source for dietary lutein. This study assessed immunomodulatory activities of the silk lutein extract. Female BALB/c mice orally received lutein, either as silk or marigold extracts (10 or 20 mg/kg daily), or vehicle only (1% tween 80 in PBS pH 7.4) for 4 weeks. Natural killer (NK) cell activity, specific antibody production, lymphocyte subpopulations, mitogen-induced lymphocyte proliferation, and cytokine production were examined. RESULTS: Silk lutein extract increased NK cell activity, and the effect was dose-related whereas marigold lutein extract was ineffective. Silk lutein extract dose-dependently enhanced antibody production in pre-immunized mice but marigold lutein extract had no effect. Feeding with silk lutein extract increased the populations of CD3+ and CD4 + CD3 + cells. Silk lutein extract also stimulated concanavalin A- and lipopolysaccharide-induced proliferations of T and B lymphocytes, respectively. Moreover, silk lutein extract increased IL-2 and IFN-γ production while the effect of marigold lutein extract was undetectable. CONCLUSIONS: Together, silk lutein extract enhanced both innate and adaptive immune functions. This preparation may prove to be an effective supplement for strengthened immunity.

Immune enhancement activities of silk lutein extract from Bombyx mori cocoons

BACKGROUND: Declining immune function poses an important clinical challenge worldwide and supplementation with natural products that possessing immune enhancing properties is a promising approach for preventing or delaying immune function decline. Cocoons from yellow silkworms are a significant source of lutein, and this unexplored silk extract could be a viable alternative source for dietary lutein. This study assessed immunomodulatory activities of the silk lutein extract. Female BALB/c mice orally received lutein, either as silk or marigold extracts (10 or 20 mg/kg daily), or vehicle only (1% tween 80 in PBS pH 7.4) for 4 weeks. Natural killer (NK) cell activity, specific antibody production, lymphocyte subpopulations, mitogen-induced lymphocyte proliferation, and cytokine production were examined. RESULTS: Silk lutein extract increased NK cell activity, and the effect was dose-related whereas marigold lutein extract was ineffective. Silk lutein extract dose-dependently enhanced antibody production in pre-immunized mice but marigold lutein extract had no effect. Feeding with silk lutein extract increased the populations of CD3+ and CD4 + CD3 + cells. Silk lutein extract also stimulated concanavalin A- and lipopolysaccharide-induced proliferations of T and B lymphocytes, respectively. Moreover, silk lutein extract increased IL-2 and IFN-γ production while the effect of marigold lutein extract was undetectable. CONCLUSIONS: Together, silk lutein extract enhanced both innate and adaptive immune functions. This preparation may prove to be an effective supplement for strengthened immunity.

Anti-oxidative, anti-tumor-promoting, and anti-carcinogensis activities of nitroastaxanthin and nitrolutein, the reaction products of astaxanthin and lutein with peroxynitrite.

Astaxanthin captured peroxynitrite to form nitroastaxanthins. 15-Nitroastaxanthin was a major reaction product of astaxanthin with peroxynitrite. Here, the anti-oxidative, anti-tumor-promoting, and anti-carcinogensis activities of 15-nitroastaxanthin were investigated. In addition to astaxanthin, 15-nitroastaxanthin showed excellent singlet oxygen quenching activity. Furthermore, 15-nitroastaxanthin showed inhibitory effects of in vitro Epstein-Barr virus early antigen activation and two-stage carcinogensis on mouse skin papillomas. These activities were slightly higher than those of astaxanthin. Similar results were obtained for the 15-nitrolutein, a major reaction product of lutein with peroxynitrite.

Dietary lutein and fat interact to modify macrophage properties in chicks hatched from carotenoid deplete or replete eggs.

Two experiments were conducted to study the interaction between dietary lutein and fat levels in broiler chicks hatched from lutein depleted (Experiment I) and repleted (Experiment II) eggs. In both experiments, a 2 x 3 factorial arrangement of treatments resulted in six dietary treatments (fat at 3% and 6% and lutein at 0, 25 and 50 mg/kg feed) that were fed for 23 days to 18 birds per treatment (in three replications). In Experiment I, the anti-dinitrophenyl-keyhole-lympet-hemocyanin (anti-DNP-KLM) serum antibody response at day 22 and macrophage phagocytotic index at day 17 did not differ among treatment groups (p > 0.05). The concavalin A and phytohaemagglutinin-P lymphocyte proliferation index at day 19 was greater in birds fed 50 mg of lutein and 3% fat than in birds fed all other diets (p < 0.05). Independent of the level of dietary fat, dietary lutein increased macrophage (day 23) nitrite production measured 46 h after in vitro stimulation with LPS (p < 0.05). Among the birds fed lutein at 25 or 50 mg/kg feed, birds fed 3% fat had higher LPS-induced nitrite production compared to the birds fed 6% fat after 46 (p = 0.014) or 70 h (p < 0.001). In Experiment II, macrophage nitrite production was measured at 54 h after LPS stimulation on days 11, 15, 19 and 23. An interaction between dietary lutein and fat levels on nitrite production was observed on day 19 (p = 0.012), where macrophages from birds fed 0 mg lutein and 3% fat had the highest nitrite production (p = 0.012). Macrophages from birds fed lutein at 25 and 50 mg/kg diet and 3% fat had higher (p = 0.012) nitrite production than birds fed 6% fat. Thus, in birds hatched from lutein deplete and replete eggs, modulation of macrophage nitrite production by lutein is dependent on the level of dietary fat.

Experimental manipulation of egg carotenoids affects immunity of barn swallow nestlings.

The yolk of bird eggs contains maternal carotenoids that may act as antioxidants thus influencing offspring performance and survival. However, to our knowledge, this hypothesis has not been subjected to experimental tests and the function of transmission of carotenoids to the egg is largely unknown. We directly manipulated the concentration of the main carotenoid (lutein) in the eggs of barn swallows (Hirundo rustica) and analysed the effect of experimental manipulation on growth of nestlings and two fundamental components of their acquired immunity. Nestlings hatched from lutein-inoculated eggs had larger T-cell-mediated immune response compared with those of two control groups. T-cell-mediated immune response predicted nestling survival until fledging. However, lutein inoculation did not affect antibody response to an immunogen, body mass, tarsus length or plumage development. Nestling body mass and plumage development declined with egg laying order, but the effects of lutein inoculation were independent of egg laying order for all traits. Our results show that maternal yolk carotenoids can have a major effect in promoting a fundamental component of immunity that predicts offspring survival and suggests that adaptive early maternal effects can be mediated by transmission of antioxidants to eggs.

Dietary lutein stimulates immune response in the canine.

The possible immuno-modulatory action of dietary lutein in dogs is not known. Female Beagle dogs (17-18-month old; 11.4+/-0.4kg body weight) were supplemented daily with 0, 5, 10 or 20mg lutein for 12 weeks. Delayed-type hypersensitivity (DTH) response to saline, phytohemagglutinin (PHA) and a polyvalent vaccine was assessed on Weeks 0, 6 and 12. Blood was sampled on Weeks 0, 2, 4, 8 and 12 to assess (1) lymphocyte proliferative response to PHA, concanavalin A (Con A), and pokeweed mitogen (PWM), (2) changes in peripheral blood mononuclear cell (PBMC) populations, (3) interleukin-2 (IL-2) production and (4) IgG and IgM production. After the completion of 12-week study, we continued to collect the blood weekly up to 17 weeks to evaluate the changes in immunoglobulin production upon first and second antigenic challenges on Weeks 13 and 15. Plasma lutein+zeaxanthin was undetectable in unsupplemented dogs but concentrations increased (P<0.05) rapidly on Week 2 in lutein-supplemented dogs. Thereafter, concentrations generally continued to increase in dose-dependent manner, albeit at a much slower rate. Dogs fed lutein had heightened DTH response to PHA and vaccine by Week 6. Dietary lutein increased (P<0.05) lymphocyte proliferative response to all three mitogens and increased the percentages of cells expressing CD5, CD4, CD8 and major histocompatibility complex class II (MHC II) molecules. The production of IgG increased (P<0.05) in lutein-fed dogs after the second antigenic challenge. Lutein did not influence the expression of CD21 lymphocyte marker, plasma IgM or IL-2 production. Therefore, dietary lutein stimulated both cell-mediated and humoral immune responses in the domestic canine.