An airbone mold-derived product, beta-1,3-D-glucan, potentiates airway allergic responses

Repeated inhalation of allergen leads to the down-regulation of allergen-sp ecific IgE responses in non-atopic individuals as well as in mice. This phe nomenon is named inhalation-induced IgE tolerance. In contrast, inhaled all ergen causes significant IgE and allergic responses in atopic persons. The mechanisms involved in this differential regulation of airway allergen-spec ific immune responses remain unclear. Besides the allergen exposure of gene tically susceptible individuals, environmental contamination is considered to play a role as an initiating factor for airway allergic responses. Using a murine model, we demonstrate here that airborne beta-1,3-D-glucan, which exists frequently in our environment, particularly in highly humid areas, can abrogate inhalation-induced IgE isotype-specific downregulation and pro mote airway eosinophil infiltration to inhaled antigen.