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首页> 外文期刊>International immunopharmacology >Luminal acetylcholine does not affect the activity of the CFTR in tracheal epithelia of pigs
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Luminal acetylcholine does not affect the activity of the CFTR in tracheal epithelia of pigs

机译：发光乙酰胆碱不影响猪气管上皮中CFTR的活性

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Fluid homeostasis mediated by the airway epithelium is required for proper lung function, and the CFTR (cystic fibrosis transmembrane conductance regulator) Cl- channel is crucial for these processes. Luminal acetylcholine (ACh) acts as an auto-/paracrine mediator to activate Cl- channels in airway epithelia and evidence exists showing that nicotinic ACh receptors activate CFTR in murine airway epithelia. The present study investigated whether or not luminal ACh regulates CFTR activity in airway epithelia of pigs, an emerging model for investigations of human airway disease and cystic fibrosis (CF) in particular. Transepithelial ion currents of freshly dissected pig tracheal preparations were measured with Ussing chambers. Application of luminal ACh (100 mu M) induced an increase of the short-circuit current (I-SC). The ACh effect was mimicked by muscarine and pilocarpine (100 mu M each) and was sensitive to muscarinic receptor antagonists (atropine, 4-DAMP, pirenzepine). No changes of the I-SC were observed by nicotine (100 mu M) and ACh responses were not affected by nicotine or mecamylamine (25 mu M). Luminal application of IBMX (I, 100 mu M) and forskolin (F, 10 mu M), increase the I-SC and the I/F-induced current were decreased by the CFTR inhibitor GlyH-101 (GlyH, 50 mu M) indicating increased CFTR activity by I/F. In contrast, GlyH did not affect the ACh-induced current, indicating that the ACh response does not involve the activation of the CFTR. Results from this study suggest that luminal ACh does not regulate the activity of the CFTR in tracheal epithelia of pigs which opposes observation from studies using mice airway epithelium. (C) 2015 Elsevier B.V. All rights reserved.
机译：正常的肺功能需要由气道上皮介导的液体稳态，而CFTR（囊性纤维化跨膜电导调节剂）Cl-通道对于这些过程至关重要。发光的乙酰胆碱（ACh）充当自体/旁分泌介质激活气道上皮中的Cl-通道，并且有证据表明烟碱型ACh受体激活鼠气道上皮中的CFTR。本研究调查了腔内ACh是否调节猪气道上皮中的CFTR活性，这是一种用于研究人类气道疾病和囊性纤维化（CF）的新兴模型。用Ussing室测量新鲜解剖的猪气管制剂的经上皮离子电流。内腔ACh（100μM）的使用引起短路电流（I-SC）的增加。毒蕈碱和毛果芸香碱（每种100μM）可模仿ACh效应，并且对毒蕈碱受体拮抗剂（阿托品，4-DAMP，哌仑西平）敏感。尼古丁（100μM）未观察到I-SC的变化，尼古丁或美卡敏（25μM）未影响ACh反应。 CFTR抑制剂GlyH-101（GlyH，50μM）降低IBMX（I，100μM）和福司可林（F，10μM）的发光应用，增加I-SC和I / F诱导的电流表明I / F增加了CFTR活动。相反，GlyH不会影响ACh诱导的电流，表明ACh反应不涉及CFTR的激活。这项研究的结果表明，管腔ACh不能调节猪气管上皮中CFTR的活性，这与使用小鼠气道上皮进行的研究相反。 （C）2015 Elsevier B.V.保留所有权利。

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