IL-33 and IL-1RL1 are well-replicated asthma genes that act in a single pathway towards type-2 immune responses. IL-33 is expressed by basal epithelial cell, and release of IL-33 upon epithelial damage can activate innate lymphoid cells, T helper-2 cells, basohilic granulocytes and mast cells through a receptor complex containing IL-1RL1. However, it is unkown how bronchial epithelial cells respond to IL-33, and whether this response is increased in disease. We aimed to characterize the IL-33-driven transcriptomic changes in cultured primary bronchial epithelial cells from patients with asthma and healthy controls. Primary bronchial epithelial cells (PBECs) were obtained by bronchial brushing. We cultured PBECs either as epithelial organoids or in air-liquid interface (ALI) conditions, followed by stimulation with recombinant IL-33, RNA-sequencing and differential gene expression analysis. We did not detect any genome-wide significant differentially expressed genes after stimulation of PBECs with IL-33, irrespective of growth in 3D epithelial organoids or after differentiation in ALI cultures. These results were identical between PBECs obtained from patients with asthma or from healthy control subjects. We detected very low levels of IL-1RL1 gene expression in these airway epithelial cell cultures. We conclude that bronchial epithelial cells do not have a transcriptional response to IL-33, independent of their differentiation state. Hence, the airway epithelium acts as a source of IL-33, but does not seem to contribute to the response upon release of the alarmin after epithelial damage.