首页> 美国卫生研究院文献>International Journal of Molecular Sciences >The Effect of Sodium Bicarbonate a Beneficial Adjuvant Molecule in Cystic Fibrosis on Bronchial Epithelial Cells Expressing a Wild-Type or Mutant CFTR Channel
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The Effect of Sodium Bicarbonate a Beneficial Adjuvant Molecule in Cystic Fibrosis on Bronchial Epithelial Cells Expressing a Wild-Type or Mutant CFTR Channel

机译:碳酸氢钠一种囊性纤维化的有益辅助分子对表达野生型或突变CFTR通道的支气管上皮细胞的影响

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摘要

Clinical and experimental results with inhaled sodium bicarbonate as an adjuvant therapy in cystic fibrosis (CF) are promising due to its mucolytic and bacteriostatic properties, but its direct effect has not been studied on respiratory epithelial cells. Our aim was to establish and characterize co-culture models of human CF bronchial epithelial (CFBE) cell lines expressing a wild-type (WT) or mutant (deltaF508) CF transmembrane conductance regulator (CFTR) channel with human vascular endothelial cells and investigate the effects of bicarbonate. Vascular endothelial cells induced better barrier properties in CFBE cells as reflected by the higher resistance and lower permeability values. Activation of CFTR by cAMP decreased the electrical resistance in WT but not in mutant CFBE cell layers confirming the presence and absence of functional channels, respectively. Sodium bicarbonate (100 mM) was well-tolerated by CFBE cells: it slightly reduced the impedance of WT but not that of the mutant CFBE cells. Sodium bicarbonate significantly decreased the more-alkaline intracellular pH of the mutant CFBE cells, while the barrier properties of the models were only minimally changed. These observations indicate that sodium bicarbonate is beneficial to deltaF508-CFTR expressing CFBE cells. Thus, sodium bicarbonate may have a direct therapeutic effect on the bronchial epithelium.
机译:吸入性碳酸氢钠作为囊性纤维化(CF)的辅助疗法的临床和实验结果很有希望,因为它具有粘液溶解和抑菌特性,但尚未对呼吸道上皮细胞进行直接研究。我们的目的是建立和表征表达野生型(WT)或突变型(deltaF508)CF跨膜电导调节剂(CFTR)通道的人CF支气管上皮(CFBE)细胞系与人血管内皮细胞的共培养模型,并研究碳酸氢盐的影响。血管内皮细胞在CFBE细胞中诱导了更好的屏障特性,这表现为更高的抵抗力和更低的渗透率值。 cAMP激活CFTR可以降低WT中的电阻,但不能降低突变CFBE细胞层中的电阻,从而分别确认功能通道的存在和不存在。碳酸氢钠(100 mM)被CFBE细胞很好地耐受:它稍微降低了WT的阻抗,但没有降低突变CFBE细胞的阻抗。碳酸氢钠显着降低了突变CFBE细胞的碱性更高的细胞内pH,而模型的阻隔性能仅发生了最小的变化。这些观察结果表明碳酸氢钠对表达deltaF508-CFTR的CFBE细胞有益。因此,碳酸氢钠可能对支气管上皮具有直接的治疗作用。

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