The pathogenesis of pollen-food allergy syndrome and therapeutic strategy in a novel murine model

Abstract

Pollen-food allergy syndrome (PFAS) is an oral allergy syndrome caused by inhalation of pollen antigens and commonly presents with local oral itching, numbness, and oral mucosal edema. These symptoms develop within several minutes of exposure to foods including fruits and vegetables; systemic symptoms such as anaphylactic shock are rare. We developed a novel PFAS murine model to analyze the underlying pathogenesis of PFAS. Birch-pollen-immunized mice were orally administered apple extract, and oral symptoms were evaluated based on oral rubbing frequency following the challenge. In the murine PFAS model, the oral rubbing frequency after the oral challenge with apple extract was significantly reduced in the birch-pollen-immunized Fcer1a^–/– mice and mast cell-deficient mice compared with the immunized wild-type mice. The apple extract stimulation did not increase the production of Th2-cytokine in the oral mucosa or the number of group 2 innate lymphoid cells or eosinophils. PFAS involves an early-phase response by mast cell degranulation via IgE signaling after the cross-reactivity of Bet v 1-specific IgE and the food allergen, and exacerbation of allergic symptoms via proteases in food; PFAS does not involve a late phase with local Th2/eosinophilic inflammation in the oral mucosa. This novel murine model might be utilized to elucidate the pathogenesis of PFAS and in the assessment of new therapeutic strategies for PFAS.