Abstract
Cow’s milk allergy is a common food allergy in infants, and is associated with an increased risk of developing other allergic diseases. Dietary selenium (Se), one of the essential micronutrients for humans and animals, is an important bioelement which can influence both innate and adaptive immune responses. However, the effects of Se on food allergy are still largely unknown. In the current study it was investigated whether dietary Se supplementation can inhibit whey-induced food allergy in an animal research model. Three-week-old female C3H/HeOuJ mice were intragastrically sensitized with whey protein and cholera toxin and randomly assigned to receive a control, low, medium or high Se diet. Acute allergic symptoms, allergen specific immunoglobulin (Ig) E levels and mast cell degranulation were determined upon whey challenge. Body temperature was significantly higher in mice that received the medium Se diet 60 min after the oral challenge with whey compared to the positive control group, which is indicative of impaired anaphylaxis. This was accompanied by reductions in antigen-specific immunoglobulins and reduced levels of mouse mast cell protease-1 (mMCP-1). This study demonstrates that oral Se supplementation may modulate allergic responses to whey by decreasing specific antibody responses and mMCP-1 release.
Highlights
Cow’s milk allergy (CMA) is one of the most common food allergies, affecting 2–3% of all infants [1]
The ear swelling in the medium Se-supplemented animals (∆ ear swelling 102 ± 22 μm) was not significantly different from the mice in the tolerance group, no significant effects of Se supplementation could be observed when these groups were compared to the positive control
30 and 60 min after the i.d. challenge in both ears, a drop in mean body temperature was observed in the sensitized animals that had not received whey in the tolerance induction phase, but only the mice in the positive control group had a significantly lower body temperature when compared to the phosphate buffered saline (PBS) and the tolerance group (Figure 2C,D)
Summary
Cow’s milk allergy (CMA) is one of the most common food allergies, affecting 2–3% of all infants [1]. In IgE-mediated CMA, about 85% of patients mostly experience mild symptoms, while 15% can develop severe allergic responses and about 9% develop anaphylaxis within minutes to hours after ingestion of cow’s milk [2,3]. No curative treatment is available for CMA and the only way to prevent allergic reactions is to avoid the intake of cow’s milk proteins. The major allergens in cow’s milk are αS1-casein from casein, and α-lactalbumin and β-lactoglobulin from whey. These proteins can be degraded in the intestines and pass through the epithelial barrier, after which they are presented to naïve T-cells by antigenpresenting cells such as dendritic cells (DC). In CMA, these T-cells differentiate into T helper 2 cells (Th2) which can drive allergic immune responses, including the expansion of eosinophils and mast cells, as well as isotype switch in B cells towards IgE production [8]
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