Damage to the airway epithelium is common in asthma. Corticosteroids induce apoptosis in and suppress proliferation of airway epithelial cells in culture. Whether apoptosis contributes to impaired epithelial cell repair after injury is not known. We examined whether corticosteroids would impair epithelial cell migration in an in vitro model of wound closure. Wounds (~ 0.5 - 1.3 mm²) were created in cultured 1HAEo^- human airway epithelial cell monolayers, after which cells were treated with up to 10 µM dexamethasone or budesonide for 24 hr. Cultured cells were pre-treated for 24 or 48 hr with dexamethasone to observe the effect of long term exposure on wound closure. After 12 hr, remaining wound area in monolayers pre-treated for 48 hr with 10 µM dexamethasone was 43 ± 18 % versus 10 ± 8 % for untreated, control monolayers. The addition of either corticosteroid immediately after injury did not slow closure significantly. After 12 hr in monolayers treated with 10 µM budesonide was 39 ± 4% versus 43 ± 3% for untreated, control monolayers. The proportion of apoptotic epithelial cells as measured by TUNEL labeling both at and away from the wound edge was higher in monolayers treated with budesonide compared to control. However, wound closure in the apoptosis-resistant 1HAEo^-.Bcl-2⁺ cell line was not different after dexamethasone treatment. We demonstrate that corticosteroid treatment prior to mechanical wounding impairs airway epithelial cell migration. The addition of corticosteroids after injury does not slow migration despite their ability to induce apoptosis in these cells.