Background – Gastro-oesophageal reflux and aspiration may be associated with lung disease. Bile acid aspiration has been shown to be prevalent among patients with advanced lung disease, which raises the concern that recurrent microaspiration of bile acids may cause lung injury. Objectives – To investigate the possible links between bile acids and lung injury using primary bronchial epithelial cell cultures taken from lung transplant patients , immortalized human bronchial epithelial cell line (BEAS- 2B) and Human lung carcinoma cells (NCI-H292) cells. Methods – Primary epithelial cells (PBECs), immortalized human bronchial epithelial cell line (BEAS- 2B) and Human lung carcinoma cells (NCI-H292) were cultured. The effect of individual primary and secondary bile acids were evaluated by 48 hour challenge. Post-challenge IL-8 and IL-6 concentrations were measured using commercial ELISAs. The viability of the (NCI-H292), (BEAS- 2B) and (PBECs) cells were measured using the Cell Titerblue assay and MTT assays. Results – Primary epithelial cells (PBECs) and Human lung carcinoma cells (NCI-H292) cells can be cultured successfully. The secondary bile acid lithocholic acid was successfully used to stimulate cultured PBECs at different concentrations from 1μmol/l to 20μmol/l. A concentration of lithocholic acid above 18μmol/l causes 100% PBEC death. Potentially physiological challenges with bile acids led to release of IL-8 from lung transplant PBECs. Human lung carcinoma cells (NCI-H292) were stimulated with lithocholic acid and Deoxycholic acid. Lithocholic acid above 20μmol/l caused 100% cell death wheras Deoxycholic acid above 50μmol/l caused 50% cell death. Conclusion – Aspiration of bile acids may cause cell damage, inflammation and cell death.