BACKGROUND In a last decade, new types of skin manifestations have been recognized in atopic dermatitis especially in Japan. They are frequently observed in adult patients with atopic dermatitis after a long-standing steroid ointment and termed adult type-atopic dermatitis. OBJECTIVE To clarify whether topical glucocorticoid (GC) modulates cutaneous inflammatory reactions in addition to known anti-inflammatory effect, we have examined the effect of long-term application of topical GC on IgE-mediated murine cutaneous reactions. METHODS Fifty microlitres of diflucortolone valerate (1 mg/mL), prednisolone valerateacetate (3 mg/mL), or triamcinolone acetonide (1 mg/mL) were applied seven times on alternate day, to the flank skin of mice. On day 12 when mice received the seventh application of GC, each mouse was given an intravenous application of IgE anti-DNP antibody (PCA titre > x 2560) 1 h before the skin test with 0.15% DNFB in acetone:olive oil (4:1) on the right pinna. The left pinna was painted with a vehicle as a control. Increased ear thickness was measured at 1, 4, 24, 48 and 72 h to assess the augmentry effect of GC. RESULTS Topical application of GC (50 microg diflucortolone valerate in ethanol) on the flank skin seven times on alternate days, augmented expression of passive cutaneous anaphylaxis reaction on the ear skin induced by intravenous applications of monoclonal IgE anti-DNP antibody and following the challenge test. In contrast, topical application of GC inhibited the reactions when applied on the challenged sites. Several types of GC, but not vitamin D3, augmented the skin reactions and these augmented reactions persisted for 72 h when control skin reactions subsided. GC induced a late phase but not an early phase cutaneous reaction in mast cell deficient WBB6F1 v/v mice by IgE anti-DNP antibody. CONCLUSIONS Long-term application of topical GC might modulate local cutaneous immune response and augment IgE-mediated cutaneous reactions. Fc epsilon R(+) cells other than mast cell might be involved in the IgE-mediated late-phase reaction.