IL-17-driven inflammation and increased levels of TNF? have been linked to pulmonary inflammatory conditions associated with corticosteroid resistance such as COPD. Physiologically relevant in vitro models of bronchial epithelial cells cultured at air-liquid interface (ALI) are becoming a tool for testing inhaled anti-inflammatory agents. This study investigates the effect of the combined exposure to IL-17 and TNF? to ALI human normal bronchial epithelial cell cultures (MucilAir?) in the presence of the inhaled corticosteroid budesonide. Upon exposure for 24h to a pro-inflammatory stimulus composed by IL-17 (30ng/ml) and TNF? (30 ng/ml), we detected a marked upregulation of various cytokines mRNA including CCL20, CCL22, CSF2, CCL2, IL-1?, CXCL1, CXCL8, which were, for the most part, resistant to modulation by budesonide. Moreover, IL-17 and TNF? induced the release of several cytokines and chemokines, such as CCL22, CCL5, CSF2 and CCL2, with only the latter being modulated by budesonide. IL-17 and TNF? induced the mRNA expression of some structural genes such as the connexins GJB2 and GJA1, an effect modulated by budesonide. IL-17 and TNF? caused a decreased of transepithelial electrical resistance (TEER) not counteracted by budesonide. In addition, IL-17 and TNF? stimulation resulted in decrease in cilia beating frequency, which was not rescued by budesonide.  In sum, the model here described mimics a corticosteroid-resistant inflammatory condition of the airway epithelium and is suitable for testing anti-inflammatory drugs in comparison and/or in combination with corticosteroids.