The present invention relates to the use of an air-liquid interface culture model using asthmatic bronchial epithelial cells, which exhibit impaired epithelial barrier function. It is proposed to use asthmatic epithelial cultures, in the absence of added Th2 or proinflammatory cytokines such as IL-13, as an in vitro model to screen for agents that can act to improve impaired asthmatic epithelial barrier function. Such agents may have therapeutic utility in asthma patients.