Allergic rhinitis (AR) is caused by an allergic reaction at nasal epithelia against allergens such as pollen and house dust. The antihistamine drugs or leukotriene receptor antagonist are used for the AR therapy, however there are some patients, who do not respond to these drugs. Hence, it needs to develop newer drugs. In this study, we focused on neuropeptides known to be involved in an inflammatory process: Gastrin-releasing peptide (GRP) and Galanin (GAL).
AR model mice were constructed as follows. The ovalbumin together with the adjuvant, aluminum hydroxide was injected into mice intraperitoneally three times every other week as primary sensitization. Then ovalbumin was administrated intraperitoneally 14 consecutive days as secondary sensitization. Allergic reactions were evaluated by the number of rubbing sneezing episodes.
GRP and its receptor, GEPR, were expressed in nasal epithelial cells and the mast cells, and their expression was increased after AR induction. A GRPR antagonist suppressed AR symptoms. GAL and its receptor, GALR2 were expressed in nasal epithelial cells and B cells. A GALR2 antagonist suppressed the level of serum IgE, numbers of B cells. It seems that the signaling of GRP and GAL may be involved in the pathophysiology of AR and their inhibition would become the new therapeutic target for AR.