Aldhahrani Adil, Verdon Bernard, Ward Chris, Pearson Jeffery
Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, UK.
Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, UK; Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK; These authors contributed equally.
ERJ Open Res. 2017 Mar 22;3(1). doi: 10.1183/23120541.00107-2016. eCollection 2017 Jan.
Gastro-oesophageal reflux and aspiration have been associated with chronic and end-stage lung disease and with allograft injury following lung transplantation. This raises the possibility that bile acids may cause lung injury by damaging airway epithelium. The aim of this study was to investigate the effect of bile acid challenge using the immortalised human bronchial epithelial cell line (BEAS-2B). The immortalised human bronchial epithelial cell line (BEAS-2B) was cultured. A 48-h challenge evaluated the effect of individual primary and secondary bile acids. Post-challenge concentrations of interleukin (IL)-8, IL-6 and granulocyte-macrophage colony-stimulating factor were measured using commercial ELISA kits. The viability of the BEAS-2B cells was measured using CellTiter-Blue and MTT assays. Lithocholic acid, deoxycholic acid, chenodeoxycholic acid and cholic acid were successfully used to stimulate cultured BEAS-2B cells at different concentrations. A concentration of lithocholic acid above 10 μmol·L causes cell death, whereas deoxycholic acid, chenodeoxycholic acid and cholic acid above 30 μmol·L was required for cell death. Challenge with bile acids at physiological levels also led to a significant increase in the release of IL-8 and IL6 from BEAS-2B. Aspiration of bile acids could potentially cause cell damage, cell death and inflammation . This is relevant to an integrated gastrointestinal and lung physiological paradigm of chronic lung disease, where reflux and aspiration are described in both chronic lung diseases and allograft injury.
胃食管反流和误吸与慢性和终末期肺部疾病以及肺移植后的同种异体移植物损伤有关。这增加了胆汁酸可能通过损伤气道上皮而导致肺损伤的可能性。本研究的目的是使用永生化人支气管上皮细胞系（BEAS-2B）来研究胆汁酸刺激的效果。培养永生化人支气管上皮细胞系（BEAS-2B）。48小时的刺激评估了单个初级和次级胆汁酸的效果。使用商用酶联免疫吸附测定试剂盒测量刺激后白细胞介素（IL）-8、IL-6和粒细胞-巨噬细胞集落刺激因子的浓度。使用CellTiter-Blue和MTT测定法测量BEAS-2B细胞的活力。石胆酸、脱氧胆酸、鹅去氧胆酸和胆酸成功用于以不同浓度刺激培养的BEAS-2B细胞。石胆酸浓度高于10μmol·L会导致细胞死亡，而脱氧胆酸、鹅去氧胆酸和胆酸浓度高于30μmol·L才会导致细胞死亡。生理水平的胆汁酸刺激也导致BEAS-2B释放IL-8和IL-6显著增加。胆汁酸的误吸可能会导致细胞损伤、细胞死亡和炎症。这与慢性肺病的综合胃肠和肺生理模式相关，在慢性肺病和同种异体移植物损伤中均描述了反流和误吸。
