Rationale Airway epithelial cells play roles in both innate immunity and inflammatory responses in the airways. To determine whether glucocorticoids regulate airway epithelial responses uniformly, we investigated the effect of the potent glucocorticoid FP on expression of both innate immune effectors and inflammatory mediators after stimulation with the Toll-like receptor 3 ligand double stranded RNA (dsRNA). Methods BEAS-2B airway epithelial cells were treated with FP (10 −7 M) for 2 hours before stimulation with dsRNA (25 μg/ml) for 18 hours. RNA was isolated for real-time RT-PCR analysis and cell supernatants were analyzed for protein by ELISA. Results In ≥3 experiments, stimulation of AEC with dsRNA increased mRNA levels as indicated: Complement factor B (mean, 28 fold), factor H (30 fold), SAA (78 fold), secretory leukocyte protease inhibitor (SLPI) (2.4 fold), RANTES (3028 fold), IL-8 (1025 fold), MIP-1α (101 fold), GM-CSF (1622 fold), IL-1β (34 fold). Treatment with FP did not inhibit induction of mRNA for factor B, factor H, SAA or SLPI. FP did inhibit expression of mRNA for IL-8, MIP-1α, RANTES, IL-1β and GM-CSF induced by dsRNA (in all cases ≥58% inhibition, n=3-5, p<0.05). Similar results were obtained in human primary bronchial epithelial cells (n=1). ELISA of SAA, GM-CSF and IL-8 confirmed the mRNA expression results. Conclusion These results suggest that glucocorticoids may spare innate immune responses in airway epithelial cells while they inhibit expression of inflammatory mediators.