<b>Introduction:</b> Inhaled glucocorticoids (corticosteroids) act on the glucocorticoid receptor (GR, NR3C1) to control inflammation in asthma by reducing the expression of inflammatory genes. This may involve direct repression of inflammatory gene transcription by GR and induction of anti-inflammatory genes. However, GR is a transcription factor that induces the expression of many genes, including other transcription factors. <b>Aims:</b> To characterize the expression of transcriptional regulators that are induced by glucocorticoids in airway epithelial cells and in the airways. <b>Methods:</b> Gene expression profiling of RNA from: i) primary human bronchial epithelial cells; ii) pulmonary A549 epithelial cells; and iii) BEAS-2B cells following budesonide treatment was performed using Affymetrix PrimeView microarrays. Data was compared to that from biopsies of healthy individuals 6 h following a single dose of inhaled budesonide. Selected genes were validated by qPCR. <b>Results:</b> Gene ontology showed up to 20% of genes upregulated by budesonide treatment in the human airways as being involved in transcription control and many of these were common with the epithelial cells. Expression of CEBPD, FOXO3, HIF3A, KLF9, KLF15, PER1, TFCP2L1, TSC22D3 and ZBTB16 were significantly upregulated in the biopsy samples and in HBE cells, with some variability between A549 and BEAS-2B, or other structural cells. <b>Conclusion:</b> The large number of transcriptional regulators induced by glucocorticoids indicates key roles in mediating downstream responses. Mechanistic studies are required to identify roles for these factors in the desirable therapeutic effects and/or unwanted side effects of glucocorticoids.