Role of selenium in IgE mediated soybean allergy development

Food allergy is a pathological immune reaction triggered by normal innocuous dietary proteins. Soybean is widely used in many food products and has long been recognized as a source of high-quality proteins. However, soybean is listed as one of the 8 most significant food allergens. The prevalence of soybean allergy is increasing worldwide and impacts the quality of life of patients. Currently, the only strategy to manage food allergy relies on strict avoidance of the offending food. Nutritional supplementation is a new prevention strategy which is currently under evaluation. Selenium (Se), as one of the essential micronutrients for humans and animals, carries out biological effects through its incorporation into selenoproteins. The use of interventions with micronutrients, like Se, might be an interesting new approach. In this review we describe the involvement of Se in a variety of processes, including maintaining immune homeostasis, preventing free radical damage, and modulating the gut microbiome, all of which may contribute to in both the prevention and treatment of food allergy. Se interventions could be an interesting new approach for future treatment strategies to manage soybean allergy, and food allergy in general, and could help to improve the quality of life for food allergic patients

Nutritional Interventions to Prevent the Development of Atopic Diseases: A Focus on Cow's Milk Allergy

In the western world the prevalence of atopic diseases such as food allergies is increasing highly significantly. One of the earliest and most prevalent food allergies occurring in the first year of life is cow's milk allergy. No treatment is available and only avoidance of the cow's milk allergens prevents the occurrence of an allergic reaction. Since cow's milk allergic children have an increased risk of developing other allergies later in life, investigating nutritional strategies to prevent the development of cow's milk allergy by developing oral tolerance is of high interest. Nutritional components such as prebiotics, probiotics, synbiotics and long-chain polyunsaturated fatty acids possess potential to support the maturation of the immune system early in life that might prevent the development of cow's milk allergy. The available research, so far, shows promising results particularly on the development of eczema. However, the preventive effects of the nutritional interventions on the development of food allergy are inconclusive. Future research may benefit from the combination of various dietary components. To clarify the preventive effects of the nutritional components in food allergy more randomized clinical trials are needed

Assessment of protein allergenicity on the basis of immune reactivity: animal models.

Because of the public concern surrounding the issue of the safety of genetically modified organisms, it is critical to have appropriate methodologies to aid investigators in identifying potential hazards associated with consumption of foods produced with these materials. A recent panel of experts convened by the Food and Agriculture Organization and World Health Organization suggested there is scientific evidence that using data from animal studies will contribute important information regarding the allergenicity of foods derived from biotechnology. This view has given further impetus to the development of suitable animal models for allergenicity assessment. This article is a review of what has been achieved and what still has to be accomplished regarding several different animal models. Progress made in the design and evaluation of models in the rat, the mouse, the dog and in swine is reviewed and discussed

Preventive effects of a combination of dietary scGOS:lcFOS and n-3 PUFA in a murine cow's milk allergy model

Objectives and Study: Cow's milk allergy (CMA) affects 2% of children younger than 4 years and no effective prevention or treatment strategies are available. The dietary components short-chain galactoand long-chain fructo-oligosaccharides (scGOS:lcFOS) and omega-3 poly-unsaturated fatty acids (n-3 PUFA) have immune regulatory capacities and have been demonstrated to reduce the allergic symptoms in a murine model of CMA, however, it is unknown if an additional effect occur when these dietary components are combined. The objective of this study was to evaluate the preventive effect of a combination of scGOS:lcFOS and n-3 PUFA on CMA development in a mouse model. Method: 3-4 weeks old C3H/HeOuJ female mice received a control or a supplemented diet with 1% (9:1) scGOS:lcFOS, 6% n-3 PUFA or a combination of 1% scGOS:lcFOS and 6% n-3 PUFA (n=12-15) from day-14. For 5 weeks (day 0-28) the mice were weekly sensitized to 20 mg cow's milk whey protein in PBS with 10 ug cholera toxin (CT) or CT only (control). Clinical parameters were measured after intradermal and oral challenge. After the mice were killed (day 43) mesenteric lymph nodes (MLN), spleen and lamina propria (LP) were isolated to measure the levels of Th1 and Th2 subsets. Serum was collected to determine levels of mouse mast cell protease 1 (mMCP-1) and antigen specific immunoglobulins. Results: The scGOS:lcFOS diet or n-3 PUFA diet reduced the acute allergic skin response significantly. The combination diet showed no significant reduction of the acute allergic skin response. All the tested diets caused no significant reduction in CMA-induced mMCP-1 and immunoglobulins IgE, IgG1 and IgG2a serum levels. Th1 and Th2 subsets in spleen, MLN and LP were neither affected by CMA nor by the dietary supplementations. Conclusion: A dietary supplementation with scGOS:lcFOS or n-3 PUFA in a preventive setting reduce the acute allergic skin response in CMA mice. No additional effect was observed when these components were combined. CMA appeared to have no influence on Th1 and Th2 subsets in spleen and gut-associated lymphoid organs

Preventive effects of a combination of dietary scGOS:lcFOS and n-3 PUFA in a murine cow's milk allergy model

Objectives and Study: Cow's milk allergy (CMA) affects 2% of children younger than 4 years and no effective prevention or treatment strategies are available. The dietary components short-chain galactoand long-chain fructo-oligosaccharides (scGOS:lcFOS) and omega-3 poly-unsaturated fatty acids (n-3 PUFA) have immune regulatory capacities and have been demonstrated to reduce the allergic symptoms in a murine model of CMA, however, it is unknown if an additional effect occur when these dietary components are combined. The objective of this study was to evaluate the preventive effect of a combination of scGOS:lcFOS and n-3 PUFA on CMA development in a mouse model. Method: 3-4 weeks old C3H/HeOuJ female mice received a control or a supplemented diet with 1% (9:1) scGOS:lcFOS, 6% n-3 PUFA or a combination of 1% scGOS:lcFOS and 6% n-3 PUFA (n=12-15) from day-14. For 5 weeks (day 0-28) the mice were weekly sensitized to 20 mg cow's milk whey protein in PBS with 10 ug cholera toxin (CT) or CT only (control). Clinical parameters were measured after intradermal and oral challenge. After the mice were killed (day 43) mesenteric lymph nodes (MLN), spleen and lamina propria (LP) were isolated to measure the levels of Th1 and Th2 subsets. Serum was collected to determine levels of mouse mast cell protease 1 (mMCP-1) and antigen specific immunoglobulins. Results: The scGOS:lcFOS diet or n-3 PUFA diet reduced the acute allergic skin response significantly. The combination diet showed no significant reduction of the acute allergic skin response. All the tested diets caused no significant reduction in CMA-induced mMCP-1 and immunoglobulins IgE, IgG1 and IgG2a serum levels. Th1 and Th2 subsets in spleen, MLN and LP were neither affected by CMA nor by the dietary supplementations. Conclusion: A dietary supplementation with scGOS:lcFOS or n-3 PUFA in a preventive setting reduce the acute allergic skin response in CMA mice. No additional effect was observed when these components were combined. CMA appeared to have no influence on Th1 and Th2 subsets in spleen and gut-associated lymphoid organs

The Interplay between the Gut Microbiome and the Immune System in the Context of Infectious Diseases throughout Life and the Role of Nutrition in Optimizing Treatment Strategies

Infectious diseases and infections remain a leading cause of death in low-income countries and a major risk to vulnerable groups, such as infants and the elderly. The immune system plays a crucial role in the susceptibility, persistence, and clearance of these infections. With 70–80% of immune cells being present in the gut, there is an intricate interplay between the intestinal microbiota, the intestinal epithelial layer, and the local mucosal immune system. In addition to the local mucosal immune responses in the gut, it is increasingly recognized that the gut microbiome also affects systemic immunity. Clinicians are more and more using the increased knowledge about these complex interactions between the immune system, the gut microbiome, and human pathogens. The now well-recognized impact of nutrition on the composition of the gut microbiota and the immune system elucidates the role nutrition can play in improving health. This review describes the mechanisms involved in maintaining the intricate balance between the microbiota, gut health, the local immune response, and systemic immunity, linking this to infectious diseases throughout life, and highlights the impact of nutrition in infectious disease prevention and treatment

Supplementation of Mice with Specific Nondigestible Oligosaccharides during Pregnancy or Lactation Leads to Diminished Sensitization and Allergy in the Female Offspring

BACKGROUND: The maternal environment and early life exposure affect immune development in offspring. OBJECTIVE: We investigated whether development of food allergy in offspring is affected by supplementing pregnant or lactating sensitized or nonsensitized mice with a mixture of nondigestible oligosaccharides. METHODS: Dams were sensitized intragastrically with ovalbumin before mating, with use of cholera toxin (CT) as an adjuvant. Nonsensitized dams received CT only. Dams were fed a control diet or a diet supplemented with short-chain galacto oligosaccharides (scGOSs), long-chain fructo oligosaccharides (lcFOSs), and pectin-derived acidic oligosaccharides (pAOSs) in a ratio of 9:1:2 at a dose of 2% during pregnancy or lactation, resulting in 7 experimental groups. After weaning, offspring were fed a control diet and ovalbumin-CT sensitized. Acute allergic skin responses (ASRs), shock symptoms, body temperature, and specific plasma immunoglobulins were measured upon intradermal ovalbumin challenge. Th2/Th1- and regulatory T cells were analyzed with use of quantitative polymerase chain reaction and flow cytometric analysis in spleen, mesenteric lymph nodes, and blood. RESULTS: Supplementing sensitized pregnant or lactating dams with scGOS/lcFOS/pAOS resulted in lower ASRs in the offspring [offspring of sensitized female mice fed experimental diet during pregnancy (S-Preg): 48 ± 2.1 μm; offspring of sensitized female mice fed experimental diet during lactation (S-Lact): 60 ± 6.2 μm] compared with the sensitized control group (119 ± 13.9 μm). In the S-Lact group, this coincided with an absence of shock symptoms compared with the offspring of sensitized female mice fed control food during pregnancy and lactation (S-Con) and S-Preg groups, and lower ovalbumin-IgG1 [S-Con: 3.8 ± 0.1 arbitrary units (AUs); S-Preg: 3.3 ± 0.1 AUs; S-Lact: 2.4 ± 0.1 AUs] and higher ovalbumin-IgG2a concentrations (S-Con: 1.1 ± 0.1 AUs; S-Preg: 0.8 ± 0.1 AUs; S-Lact: 2.0 ± 0.1 AUs). Supplementing nonsensitized pregnant or lactating dams with scGOS/lcFOS/pAOS resulted in lower plasma ovalbumin-IgE [offspring of nonsensitized female mice fed experimental diet during pregnancy (NS-Preg): 1.6 ± 0.4 AUs; offspring of nonsensitized female mice fed experimental diet during lactation (NS-Lact): 0.3 ± 0.1 AUs vs. offspring of nonsensitized female mice fed control food during pregnancy and lactation (NS-Con): 3.1 ± 0.6 AUs] and ovalbumin-IgG1 (NS-Lact: 2.3 ± 0.3 AUs vs. NS-Con: 3.4 ± 0.3 AUs) concentrations in offspring. Ovalbumin-IgG2a plasma concentrations were higher in offspring of scGOS/lcFOS/pAOS-supplemented dams (NS-Preg: 1.1 ± 0.1 AUs; NS-Lact: 1.1 ± 0.1 AUs) than in those of unsupplemented, nonsensitized controls (0.4 ± 0.0 AUs). CONCLUSIONS: These data show impaired sensitization in offspring of scGOS/lcFOS/pAOS-supplemented mice. A number of the analyzed variables are differentially affected by whether supplementation occurs during pregnancy or lactation, and the outcome of dietary supplementation is affected by whether the mother has been sensitized to ovalbumin and CT

Supplementation of Mice with Specific Nondigestible Oligosaccharides during Pregnancy or Lactation Leads to Diminished Sensitization and Allergy in the Female Offspring

BACKGROUND: The maternal environment and early life exposure affect immune development in offspring. OBJECTIVE: We investigated whether development of food allergy in offspring is affected by supplementing pregnant or lactating sensitized or nonsensitized mice with a mixture of nondigestible oligosaccharides. METHODS: Dams were sensitized intragastrically with ovalbumin before mating, with use of cholera toxin (CT) as an adjuvant. Nonsensitized dams received CT only. Dams were fed a control diet or a diet supplemented with short-chain galacto oligosaccharides (scGOSs), long-chain fructo oligosaccharides (lcFOSs), and pectin-derived acidic oligosaccharides (pAOSs) in a ratio of 9:1:2 at a dose of 2% during pregnancy or lactation, resulting in 7 experimental groups. After weaning, offspring were fed a control diet and ovalbumin-CT sensitized. Acute allergic skin responses (ASRs), shock symptoms, body temperature, and specific plasma immunoglobulins were measured upon intradermal ovalbumin challenge. Th2/Th1- and regulatory T cells were analyzed with use of quantitative polymerase chain reaction and flow cytometric analysis in spleen, mesenteric lymph nodes, and blood. RESULTS: Supplementing sensitized pregnant or lactating dams with scGOS/lcFOS/pAOS resulted in lower ASRs in the offspring [offspring of sensitized female mice fed experimental diet during pregnancy (S-Preg): 48 ± 2.1 μm; offspring of sensitized female mice fed experimental diet during lactation (S-Lact): 60 ± 6.2 μm] compared with the sensitized control group (119 ± 13.9 μm). In the S-Lact group, this coincided with an absence of shock symptoms compared with the offspring of sensitized female mice fed control food during pregnancy and lactation (S-Con) and S-Preg groups, and lower ovalbumin-IgG1 [S-Con: 3.8 ± 0.1 arbitrary units (AUs); S-Preg: 3.3 ± 0.1 AUs; S-Lact: 2.4 ± 0.1 AUs] and higher ovalbumin-IgG2a concentrations (S-Con: 1.1 ± 0.1 AUs; S-Preg: 0.8 ± 0.1 AUs; S-Lact: 2.0 ± 0.1 AUs). Supplementing nonsensitized pregnant or lactating dams with scGOS/lcFOS/pAOS resulted in lower plasma ovalbumin-IgE [offspring of nonsensitized female mice fed experimental diet during pregnancy (NS-Preg): 1.6 ± 0.4 AUs; offspring of nonsensitized female mice fed experimental diet during lactation (NS-Lact): 0.3 ± 0.1 AUs vs. offspring of nonsensitized female mice fed control food during pregnancy and lactation (NS-Con): 3.1 ± 0.6 AUs] and ovalbumin-IgG1 (NS-Lact: 2.3 ± 0.3 AUs vs. NS-Con: 3.4 ± 0.3 AUs) concentrations in offspring. Ovalbumin-IgG2a plasma concentrations were higher in offspring of scGOS/lcFOS/pAOS-supplemented dams (NS-Preg: 1.1 ± 0.1 AUs; NS-Lact: 1.1 ± 0.1 AUs) than in those of unsupplemented, nonsensitized controls (0.4 ± 0.0 AUs). CONCLUSIONS: These data show impaired sensitization in offspring of scGOS/lcFOS/pAOS-supplemented mice. A number of the analyzed variables are differentially affected by whether supplementation occurs during pregnancy or lactation, and the outcome of dietary supplementation is affected by whether the mother has been sensitized to ovalbumin and CT