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IL-13 enhances agonist-evoked calcium signals and contractile responses in airway smooth muscle.

机译:IL-13可增强激动剂引起的钙信号和气道平滑肌的收缩反应。

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摘要

Growing evidence suggests that interleukin (IL)-13, a Th2-type cytokine, plays a critical role in the development of bronchial hyper-responsiveness (BHR), an essential feature of asthma, although the underlying mechanisms remain unknown. In the present study, we investigated whether IL-13 directly affects airway smooth muscle (ASM) function. In murine tracheal rings, IL-13 (100 ng ml-1, 24 h) significantly increased both the carbachol- and KCl-induced maximal force generation without affecting ASM sensitivity. In cultured human ASM cells, IL-13 (50 ng ml-1, 24 h) also augmented cytosolic calcium levels to bradykinin, histamine and carbachol by 60, 35 and 26%, respectively. The present study demonstrates that IL-13 may promote BHR by directly modulating ASM contractility, an effect that may be due to enhanced G protein-coupled receptor (GPCR)-associated calcium signaling.
机译:越来越多的证据表明,Th2型细胞因子白介素(IL)-13在支气管高反应性(BHR)(哮喘的基本特征)的发展中起着关键作用,尽管其潜在机制尚不清楚。在本研究中,我们调查了IL-13是否直接影响气道平滑肌(ASM)功能。在鼠气管环中,IL-13(100 ng ml-1,24 h)显着增加了卡巴胆碱和KCl诱导的最大力产生,而不会影响ASM敏感性。在培养的人ASM细胞中,IL-13(50 ng ml-1,24 h)也使缓激肽,组胺和卡巴胆碱的胞质钙水平分别增加了60%,35%和26%。本研究表明,IL-13可能通过直接调节ASM收缩力来促进BHR,这可能是由于增强的G蛋白偶联受体(GPCR)相关的钙信号传导所致。

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