Allergic rhinitis and inflammation: the effect of nasal corticosteroid therapy

Abstract

Topical corticosteroids have proved to be effective in the treatment of allergic rhinitis. The symptomatology of allergic rhinitis is considered to be the result of the accumulation and activation of inflammatory cells and cytokine release and hence the efficacy of corticosteroids is associated with their anti‐inflammatory action. New advances in allergic inflammation now suggest that not only mast cells and eosinophils but also T‐lymphocytes and antigen‐presenting dendritic cells, play an important role in the inflammatory reaction. The effect of topical fluticasone propionate on cellular infiltration in the nasal mucosa is examined, with an emphasis on two studies performed in Rotterdam, The Netherlands. The cells influenced most by corticosteroid therapy were Langerhans' cells (antigen‐presenting cells), which were almost completely eradicated, possibly resulting in diminished antigen presentation, and eosinophils. There was a reduction in the number of epithelial mast cells, but the number of T‐lymphocytes only decreased following high doses of corticosteroid therapy or long‐term treatment. However, T‐lymphocyte function was influenced, as shown by the reduction in the T‐helper, (Th_J‐related cytokines, interleukin (1L)‐4 and IL‐5. Topical corticosteroid therapy had no effect on the accumulation of macrophages. The reduction in antigen presentation, and the decrease in T‐lymphocyte stimulation and cytokine production, may cause a reduced influx of eosinophils and other inflammatory cells, resulting in diminished symptomatology.