Mechanistic analysis of experimental food allergen-induced cutaneous reactions

Individuals with food allergy often present with uritcaria and atopic dermatitis. Indeed, susceptibility to food allergy may predispose to the development of these cutaneous allergic disorders. Recently, we developed a model of food allergy, whereby oral consumption of food [pea Pisum sativum L.; expressing α-amylase inhibitor-1 (αAI) from the common bean Phaseolus vulgaris L. cv Tendergreen (pea-αAI)] promotes a T helper cell type 2 (Th₂) inflammatory response and predisposes to cutaneous allergic reactions following subsequent food allergen (αAI) exposure. To delineate the kinetics of food allergen-induced cutaneous reactions and examine the inflammatory mechanisms involved in this allergic reaction, we used interleukin (IL)-13-, IL-4 receptor α-, and eotaxin-1-deficient mice and performed serum transfer and CD4⁺ T cell depletion studies. We demonstrate that consumption of pea-αAI promotes an αAI-specific immunoglobulin G₁ (IgG₁) and IgE antibody response. Furthermore, we show that subsequent food allergen (αAI) challenge in the skin induced an early (3 h)- and late-phase (24 h) cutaneous allergic reaction. The early-phase response was associated with mast cell degranulation and the presence of Ig, whereas the late-phase response was characterized by a lymphoid and eosinophilic infiltrate, which was critically regulated by CD4⁺ T cells, IL-13, and eotaxin-1. Collectively, these studies demonstrate that food allergy can predispose to cutaneous inflammatory reactions, and these processes are critically regulated by Th₂ immune factors.