Topical glucocorticoid augments both allergic and non-allergic cutaneous reactions in mice when applied at the afferent stage of contact sensitivity

Using a murine model, topical application of glucocorticoid ([GC], 50 μg diflucortolone valerate in ethanol) on a sensitized site (flank skin) for 7 times before and 2 times after sensitization on alternate days, augmented expression of contact sensitivity reactions on the challenged site (ear skin). This augmentation was due to the systemic effect of percutaneously absorbed GC, because topical GC also augmented the skin reaction in mice that had been sensitized on a separate site from that of the GC application. In contrast, topical application of GC inhibited the contact sensitivity skin reaction when applied on the challenged sites. Intraperitoneal injection of the same dose of GC also failed to augment the skin reactions. Glucocorticoid augmented the contact sensitivity skin reactions and these persisted for 96 h after the control skin reactions subsided. Early phase (1–6 h) skin reactions were also induced or augmented when dinitrofluorobenzene or trinitrochlorobenzene but not oxazolone were used as the sensitizer; GC also augmented the non-specific reactions to croton oil or to suboptimal concentration of hapten in normal mice. The numbers of Langerhans cells (LC) were reduced in both the GC-application and challenged sites. Haptenated LC from GC-treated skin showed a rather weak sensitizing ability, which was not statistically significant. Transfer of lymph node cells and/or spleen cells or serum from GC-pre-treated mice failed to induce a contact sensitivity reaction in normal recipient mice. These results suggest that topical GC might augment cutaneous inflammation through a possible modulation of local cytokine production, regardless of the number of LC or the presence of sensitized lymphocytes