Evaluation of a microbiome-based method to protect against anaphylaxis in an infant microbiome-associated mouse model of peanut allergy

---

Presentation Time: 02:15 PM - 03:30 PM
Poster Board Number: B734
Abstract ID: 4145

Presenting Author:
Morgan Cade , Graduate Research Assistant at Univ. of Nebraska, Lincoln

Abstract:

Early-life immune programming mediated by the microbiome may influence food allergies development, potentially explaining the rapidly increasing prevalence of pediatric peanut allergy. Bifidobacterium species, notably B. longum subsp. infantis (Bif), dominate the breastfed infant gut microbiome by metabolizing abundant nondigestible human milk oligosaccharides (HMO) in breastmilk. Treatment with Bifidobacterium has induced oral tolerance in conventional mouse models of food allergy; however, it has not been tested in mice harboring a human infant gut microbiome. We hypothesized that treatment with Bif+HMO would limit the severity of anaphylaxis in an infant microbiome-associated mouse model of peanut allergy. Germ-free mice received a human infant fecal microbiome low in Bif and were orally sensitized to peanut adjuvanted with cholera toxin. Beginning at colonization, mice were gavaged with either Bif or PBS and given drinking water with or without HMO. Treatment with Bif+HMO increased Bif abundance and cecal levels of acetate and lactate compared to Bif alone. Anaphylactic scores were significantly decreased in mice given Bif+HMO versus Bif only; however, peanut-specific IgE production was significantly increased. No differences were observed in plasma mast cell protease-1 or in splenic Tregs. These results suggest HMO treatment enhances the ability of B. infantis to increase antigen-specific IgE production yet still limit innate immune responses related to anaphylaxis.