Maternal and early-life vitamin D deficiency enhances allergic reaction in an ovalbumin-sensitized BALB/c mouse model

Background: 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 developme...

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Bibliographic Details
Main Authors: Jiang Wu, Yan Zhong, Xiuhua Shen, Kefeng Yang, Wei Cai
Format: Article
Language:English
Published: Swedish Nutrition Foundation 2018-05-01
Series:Food & Nutrition Research
Subjects:
Online Access:http://foodandnutritionresearch.net/index.php/fnr/article/view/1401/4754
Description
Summary:Background: 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. Design: BALB/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. Results: Increased 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. 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.
ISSN:1654-661X