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