IgE mediated Type 2 inflammation of the Laryngopharynx
Though AL is not yet widely accepted as a form or phenotype of airway
allergy, the capacity for the laryngopharynx to mount a type 2 IgE
mediated inflammatory reaction in the presence of inhaled allergens
appears plausible, bolstered by observed eosinophilic inflammatory
reactions in several small human and animal provocation
studies[14, 16, 23]. The laryngopharynx, in
keeping with its continuity with nasal and bronchial airways, is
populated with mast cells and goblet cells[19, 20,23], and the laryngeal inlet by virtue of its function is
routinely exposed to deposition of inhaled particulates and antigens,
exacerbated in patients with nasal allergy and resulting nasal
obstruction. Further investigation is required to determine the
significance of potential primary mucosal-allergen interactions in this
setting, given implications both for therapy and for united airway
interactions.