Laboratoire de Physiologie, EA2689, IMPRT IFR 114, Université de Lille, Lille cedex, France.
J Cyst Fibros. 2013 Jan;12(1):60-7. doi: 10.1016/j.jcf.2012.06.007. Epub 2012 Jul 17.
Pseudomonas aeruginosa airway infection is associated with a high mortality rate in cystic fibrosis. Lipopolysaccharide (LPS), a main constituent of the outer membrane of P. aeruginosa, is responsible for activation of innate immune response but its role on airway epithelium ion transport, is not well known. The aim of this study was to determine the role for P. aeruginosa LPS in modulating chloride secretion and intracellular calcium in the human bronchial epithelial cell line, 16HBE14o-.
We used intracellular calcium imaging and short-circuit current measurement upon exposure of cells to P. aeruginosa LPS.
Apical LPS stimulated intracellular calcium release and calcium entry and enhanced chloride secretion. This latter effect was significantly inhibited by CFTR(inh)-172 and BAPTA-AM (intracellular Ca(2+) chelator).
Our data provides evidence for a new role of P. aeruginosa LPS in stimulating calcium entry and release and a subsequent chloride secretion via CFTR in human bronchial epithelium.
铜绿假单胞菌气道感染与囊性纤维化的高死亡率有关。脂多糖（LPS）是铜绿假单胞菌外膜的主要成分，负责激活先天免疫反应，但它在气道上皮细胞离子转运中的作用尚不清楚。本研究旨在确定铜绿假单胞菌 LPS 在调节人支气管上皮细胞系 16HBE14o-中氯离子分泌和细胞内钙方面的作用。
我们使用细胞内钙成像和短路电流测量方法来检测细胞暴露于铜绿假单胞菌 LPS 后的反应。
LPS 刺激细胞内钙释放和钙内流，并增强氯离子分泌。这种作用被 CFTR(inh)-172 和 BAPTA-AM（细胞内 Ca(2+) 螯合剂）显著抑制。
我们的数据为铜绿假单胞菌 LPS 通过 CFTR 刺激钙离子内流和释放以及随后的氯离子分泌在人支气管上皮细胞中的新作用提供了证据。
