Mouse Models of Food Allergy in the Pursuit of Novel Treatment Modalities.

Johanna M Smeekens,Michael D Kulis

doi:10.3389/falgy.2021.810067

Johanna M Smeekens, Michael D Kulis

Open Access

https://doi.org/10.3389/falgy.2021.810067

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Abstract

The prevalence of IgE-mediated food allergies has increased dramatically in the past three decades, now affecting up to 10% of the US population. IgE-mediated food allergy is an immunologic disease, involving a variety of cells, including B and T cells, mast cells, basophils, ILC2s, and epithelial cells. Mouse models of food allergy mimic the overall immunologic processes known to exist in humans. Due to the limitations of invasive sampling of human tissue and the similarities of the human and mouse immune systems, comprehensive pathogenesis studies of food allergy have been performed in mouse models. Mouse models have been effective in elucidating the roles of non-oral routes of sensitization and identifying key cells and molecules involved in allergic sensitization. Furthermore, the development of novel therapeutic approaches for food allergy has been accelerated through the use of pre-clinical mouse models. Despite the groundbreaking findings stemming from research in mice, there are continued efforts to improve the translational utility of these models. Here, we highlight the achievements in understanding food allergy development and efforts to bring novel treatment approaches into clinical trials.

Highlights

IgE-mediated food allergies affect an estimated 10% of the US population [1], which is a substantial increase from estimates generated over 20 years ago [2]
cholera toxin (CT) and staphylococcal enterotoxin B (SEB) are co-administered with food proteins through the GI tract [12, 13], while allergens adsorbed to alum are delivered via intraperitoneal injection [14]
We have recently demonstrated that CC027/GeniUnc mice become allergic to peanut and walnut without a Th2-skewing adjuvant, and sensitization is associated with increased gut permeability, decreased fecal IgA and a unique gut microbiome [17]

Summary

INTRODUCTION

IgE-mediated food allergies affect an estimated 10% of the US population [1], which is a substantial increase from estimates generated over 20 years ago [2]. CT and SEB are co-administered with food proteins through the GI tract [12, 13], while allergens adsorbed to alum are delivered via intraperitoneal injection [14] The use of these adjuvants have led to models of allergy to peanut, milk, egg, tree nuts, shellfish, among others, in BALB/c, C3H/HeJ and C57BL/6 mice, demonstrated by the production of allergen-specific IgE, Th2 cytokines and anaphylaxis upon food challenge [9]. Mice were exposed to peanut for an additional 5 weeks to induce peanut-specific IgE production These models highlight the possibility of studying food allergy in vivo using human cells

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Findings

DISCUSSION