Probiotics Prevents Sensitization to Oral Antigen and Subsequent Increases in Intestinal Tight Junction Permeability in Juvenile-Young Adult Rats.

Tulyeu Tulyeu,Yokoyama Yokoyama,Mieno Mieno,Watanabe Watanabe,Kumagai Kumagai,Cui Cui,Jimbo Jimbo,Osaka Osaka,Yamagata Yamagata

doi:10.3390/microorganisms7100463

Abstract

Increased intestinal permeability is thought to underlie the pathogenesis of food allergy. We explore the mechanism responsible for changes in the morphology and function of the intestinal barrier using a rat model of food allergy, focusing on the contribution of intestinal microbiota. Juvenile–young adult rats were sensitized with ovalbumin and treated with antibiotics or probiotics (Clostridium butyricum and Lactobacillus reuteri), respectively. The serum ovalbumin-IgE levels, intestinal permeability, histopathological features, tight junction (TJ)-associated proteins, Th2 cytokines, and gut microbiota in feces were analyzed in each group. Sensitized rats showed an increase in ovalbumin-IgE levels and intestinal permeability with gut mucosal inflammation, whereas rats that received probiotics were only mildly affected. Rats given ovalbumin, but not those given probiotics, showed a reduction in both TJ-related protein expression and localization. Th2 cytokine levels were increased in the sensitized rats, but not in those given probiotics. TJs in rats treated with ovalbumin and antibiotics were disrupted, but those in rats administered probiotics were undamaged. Clostridiaceae were increased in the probiotics groups, especially Alkaliphilus, relative to the ovalbumin-sensitized group. Gut microbiota appears to play a role in regulating epithelial barrier function, and probiotics may help to prevent food sensitization through the up-regulation of TJ proteins.

Highlights

Food allergy, the pathogenesis of which is still unknown, has become a serious public health issue, as its prevalence has increased over the last two decades and around 10% of children are affected [1]
It is reported that intestinal permeability may increase when the intestinal mucosal barrier function is damaged during allergy, and that such epithelial barrier dysfunction leads to excessive transport of macromolecular substances, which are absorbed into the deep tissues and have the potential to induce antigen-related intestinal inflammation or hypersensitivity [25,26,27,28]
A previous report has indicated that elevated expression of claudin-2 in epithelial cells plays an important role in epithelial barrier dysfunction as well as the pathogenesis of intestinal antigen-specific hypersensitivity [39], we found no significant increase of claudin-2 expression in the present study

Summary

Introduction

The pathogenesis of which is still unknown, has become a serious public health issue, as its prevalence has increased over the last two decades and around 10% of children are affected [1]. The Food Allergy and Anaphylaxis Guidelines of the European Academy of Allergy and Clinical Immunology state “there is no evidence to recommend prebiotics or probiotics or other dietary supplements based on particular nutrients to prevent food allergy” [3]. The number of reports on both basic experiments and clinical trials designed to clarify the effects of probiotics or gut microbiota on allergic disorders has been increasing [4,5,6,7,8,9,10,11,12]. Preand postnatal Lactobacillus reuteri supplementation decreases allergen responsiveness in infancy [14]. These probiotics (C. butyricum and L. reuteri) have been widely used for their expected health benefits, evidence for their effectiveness against food allergy is still insufficient

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