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首页> 外文期刊>Life sciences >Dysfunction of the non-neuronal cholinergic system in the airways and blood cells of patients with cystic fibrosis.
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Dysfunction of the non-neuronal cholinergic system in the airways and blood cells of patients with cystic fibrosis.

机译：囊性纤维化患者的气道和血细胞中非神经胆碱能系统功能异常。

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The non-neuronal cholinergic system is widely expressed in human airways, skin and immune cells. Choline acetyltransferase (ChAT), acetylcholine and nicotine/muscarine receptors are demonstrated in epithelial surface cells, submucosal glands, airway smooth muscle fibres and immune cells. Moreover, acetylcholine is involved in the regulation of cell functions like proliferation, differentiation, migration, organization of the cytoskeleton, cell-cell contact, secretion and transport of ions and water. Cystic fibrosis (CF), the most frequent genetic disorder, is known to be caused by a mutation of the CF-gene coding for the cystic fibrosis transmembrane regulator protein (CFTR). CFTR represents a regulating transport protein for ion channels and processes involving endo- and exocytosis. Despite the identification of the genetic mutation knowledge of the underlying cellular pathways is limited. In the present experiments the cholinergic system was investigated in the peripheral blood and in the lung of CF patients undergoing lung transplantation (n=7). Acetylcholine content in bronchi and lung parenchyma of CF was reduced by 70% compared to controls (tumor-free tissue obtained from patients with lung tumor; n=13). In contrast, ChAT activity was elevated to some extent (p>0.05) in CF, and esterase activity did not differ from control. Acetylcholine content extracted from peripheral leucocytes (30 ml) was also reduced by 70% in CF (n=13) compared to healthy volunteers (n=9). Double labelling experiments with anti-CF antibodies and anti-ChAT antibodies showed a co-localization in peripheral lymphocytes, giving first evidence that CFTR may be linked with the intracellular storage/transport of non-neuronal acetylcholine. It is concluded that the non-neuronal cholinergic system is involved in the pathogenesis of CF. A reduced content of non-neuronal acetylcholine could contribute to the deleterious changes of epithelial ion and water movements in CF, because acetylcholine stimulates apical Cl(-) secretion, inhibits apical Na(+) and water absorption and therewith facilitates mucociliary clearance.
机译：非神经胆碱能系统在人的气道，皮肤和免疫细胞中广泛表达。在上皮表面细胞，粘膜下腺，气道平滑肌纤维和免疫细胞中证实了胆碱乙酰基转移酶（ChAT），乙酰胆碱和烟碱/毒蕈碱受体。此外，乙酰胆碱参与细胞功能的调节，例如增殖，分化，迁移，细胞骨架的组织，细胞与细胞的接触，离子和水的分泌和运输。囊性纤维化（CF）是最常见的遗传疾病，是由编码囊性纤维化跨膜调节蛋白（CFTR）的CF基因突变引起的。 CFTR代表涉及内吞和胞吐作用的离子通道和过程的调节转运蛋白。尽管鉴定了遗传突变，但基本细胞途径的知识仍然有限。在本实验中，研究了接受肺移植的CF患者的外周血和肺中的胆碱能系统（n = 7）。与对照（从患有肺肿瘤的患者获得的无肿瘤组织; n = 13）相比，CF的支气管和肺实质中的乙酰胆碱含量降低了70％。相反，CF中ChAT活性有所提高（p> 0.05），酯酶活性与对照无差异。与健康志愿者（n = 9）相比，从外周血白细胞（30 ml）中提取的乙酰胆碱含量也降低了70％（n = 13）。用抗CF抗体和抗ChAT抗体进行的双标记实验显示了外周淋巴细胞中的共定位，这首次证明CFTR可能与非神经元乙酰胆碱的细胞内存储/运输有关。结论是非神经胆碱能系统参与CF的发病机制。减少非神经元乙酰胆碱的含量可能有助于CF中上皮离子和水运动的有害变化，因为乙酰胆碱会刺激根尖的Cl（-）分泌，抑制根尖的Na（+）和水吸收，从而促进粘膜纤毛清除。

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