Mode of action of intranasal corticosteroids

The mode of action of intranasal corticosteroids (INCS) is complex. It is n ot known whether INCS penetrate the nasal mucosa or act on target cells; ho wever, their low systemic activity supports the concept of local action on nasal mucosa. This local effect can nonetheless influence a variety of infl ammatory cells and their mediators such as epithelial cells, lymphocytes, b asophils, mast cells, and Langerhans cells. Corticosteroid-induced inhibiti on of immunoglobulin E-dependent release of histamine is a possible but unp roven mode of action. Epithelial cells are an important target for corticos teroids, and INCS concentration is high at the epithelial surface. INCS may combine with the corticosteroid receptors in epithelial cells, which are t hen expelled into the airway lumen together with the dead epithelial cells or migrating inflammatory cells. A reduced influx of mediator cells may exp lain some of the effects of INCS on rhinitis symptoms, but it cannot explai n all of the effects because INCS also reduce the early-phase sneezing and rhinorrhea after an allergen challenge outside the pollen season. In this s ituation, the number of surface mast cells/basophils is very I low, as it i s in the absence of allergic rhinitis. The mechanism by which INCS treatmen t of allergic rhinitis reduces itching, sneezing, and rhinorrhea, the chara cteristic symptoms of an early-phase response involving mast cell release o f histamine, remains to be determined. Studies should be conducted to chara cterize the broad range of mechanisms by which INCS produce their therapeut ic effects in allergic rhinitis.