Abstract

BackgroundRecent studies have shown that vitamin D deficiency may contribute to the high prevalence of food allergy but the underlying mechanisms are far from clear.ObjectiveThe present study was designed to investigate the effect of maternal and early-life vitamin D deficiency in the development of food allergy.DesignBALB/c mice were treated with ovalbumin (OVA) to trigger allergic reactions, under vitamin D-deficient (by maternal and early-life feeding of vitamin D deprived chow diet) or vitamin D-sufficient conditions.ResultsIncreased occurrence and severity of allergic diarrhea as well as decreased rectal temperature were observed after OVA sensitization. For vitamin D deficiency groups, OVA-specific IgE and IL-4 levels were significantly increased, while IFN-γ levels were unchanged. Vitamin D deficiency also attenuated the structure of small intestinal villi and decreased the expression of the tight junction protein between adjacent epithelial cells and the percentages of CD4+CD25+Foxp3+Treg cell in spleen and mesenteric lymph nodes.ConclusionsMaternal and early-life vitamin D deficiency have notable influence on the susceptibility to food allergy, which may relate with the reduced population of Treg cell and the dysfunction of intestinal epithelial barrier.

Highlights

  • Recent studies have shown that vitamin D deficiency may contribute to the high prevalence of food allergy but the underlying mechanisms are far from clear

  • The body weight of offspring at the age of 6 weeks in each group did not differ from each either. These results indicate that vitamin D deficiency did not exert obvious influence on gestational and birth outcomes, offspring mortality, and prematurity

  • Serum levels of 25(OH)D3 in standard chow diet (SC)/VD, VD-/SC, and VD-/ VD- groups were significantly decreased when compared with standard chow-fed offspring of SC-fed dams (SC/SC) group, and VD-/VD- group had the lowest level of 25(OH)D3 (Fig. 1b)

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Summary

Introduction

Recent studies have shown that vitamin D deficiency may contribute to the high prevalence of food allergy but the underlying mechanisms are far from clear. Objective: The present study was designed to investigate the effect of maternal and early-life vitamin D ­deficiency in the development of food allergy. For vitamin D deficiency groups, OVA-specific IgE and IL-4 levels were significantly increased, while IFN-γ levels were unchanged. Vitamin D deficiency attenuated the structure of small intestinal villi and decreased the expression of the tight junction protein between adjacent epithelial cells and the percentages of CD4+CD25+Foxp3+Treg cell in spleen and mesenteric lymph nodes. Conclusions: Maternal and early-life vitamin D deficiency have notable influence on the susceptibility to food allergy, which may relate with the reduced population of Treg cell and the dysfunction of intestinal epithelial barrier

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