Dicaine represses apoptosis-linked gene 2-interacting protein X expression to induce airway epithelial barrier dysfunction.

Epithelial barrier dysfunction is associated with a number of inflammatory disorders. However, the pathogenesis of epithelial barrier dysfunction is unclear. This study aims to elucidate the involvement of dicaine in airway epithelial barrier dysfunction. In the present study, an RPMI2650 (Rpc) human airway epithelial cell line was cultured, with or without dicaine, in monolayers using Transwells. In order to assess airway epithelial barrier function, the levels of transepithelial electrical resistance and permeability to ovalbumin (OVA) were measured. Expression of apoptosis-linked gene 2-interacting protein X (Alix) in Rpc cells was assessed using quantitative reverse transcription‑polymerase chain reaction and western blotting. The antigenicity of OVA was assessed using a T cell proliferation assay. The results of the present study demonstrated that Alix expression levels were markedly lower in Rpc cells treated with dicaine, compared with those not treated with dicaine. An increase in the level of transcellular permeability to OVA was observed in Rpc monolayers following treatment with dicaine, compared with that in the Rpc monolayer without dicaine treatment. Furthermore, the Rpc monolayer maintained high antigenicity and induced antigen specific T cell proliferation. In conclusion, dicaine causes a decrease in expression levels of Alix, which resulted in compromise of the Rpc cell monolayer epithelial barrier function.