Commensal microbiota regulate human health and homeostasis through a variety of mechanisms. Modern lifestyle factors deplete populations of beneficial microbes, and this dysbiosis has been correlated with the rising incidence of numerous noncommunicable chronic diseases. Re-introduction of rationally selected, protective bacteria (or their products) will likely be an effective strategy to prevent or treat these diseases by targeting the underlying cause of immune dysregulation. Our group has previously characterized the bacterial communities in the feces of food allergic patient cohorts and demonstrated a marked lack of Clostridial taxa compared to healthy counterparts. Commensal Clostridia regulate host immunity through many mechanisms, one of which is the production of butyrate. Further work from our laboratory demonstrated that healthy infant microbiotas, a single Clostridial species (Anaerostipes caccae), or butyrate can protect against the allergic response to food in murine models. We now seek to expand on this knowledge by optimizing delivery of A. caccae as a biotherapeutic to mice with dysbiotic microbiota. We outline the isolation of a novel substrain, A. caccae LAHUC, from the feces of a healthy infant and the characterization of this strain in vitro. We then discuss various mechanisms by which commensal microbiota or their products (e.g., butyrate) can modulate the host, focusing on intestinal barrier integrity. Finally, we establish that a synbiotic composed of A. caccae LAHUC and lactulose increases luminal butyrate in mice with a dysbiotic microbiota (gnotobiotic mice colonized with feces derived from an allergic infant or antibiotic treated mice). This synbiotic formulation both prevents and treats allergic responses to food in various models and microbial contexts, and we demonstrate innate and adaptive immune mechanisms for this effect. Together this thesis describes the pathway towards development of an A. caccae synbiotic, a novel therapeutic strategy for food allergy.