Commensal bacteria induce a barrier protective response to prevent sensitization to food allergens

Abstract

Environmentally-induced alterations in the commensal microbiome have been implicated in the increasing prevalence of food allergy. We found that antibiotic treatment of neonatal mice leads to reduced proportions of regulatory T cells (Tregs) in the colonic lamina propria(LP), impaired production of intestinal IgA, and elevated peanut (PN) specific IgE/IgG1 in response to sensitization. Selective colonization of gnotobiotic mice linked the Treg/IgA inducing capacity to a consortium of bacteria within the Clostridia class. Introduction of either a conventional SPF microbiota or a mixture of Clostridia strains to antibiotic-treated mice restored the Treg and IgA compartments and blocked the induction of a food allergic response. Clostridia colonized gnotobiotic mice displayed increased expression of IL-23 and IL-22 in the colonic LP compartment and the induction of anti-microbial REG3β expression in the epithelium. Collectively, these results suggest that the maintenance of oral tolerance to dietary antigens relies on bacterial populations that induce a barrier protective response, which includes activation of the IL-23/IL22 axis and the expansion of intestinal Tregs and IgA secreting B cells. Our findings hold promise for the development of approaches to prevent or treat food allergy based on modulation of the composition of intestinal microbiota.

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