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咳嗽超敏反应的外周和中枢机制。

Peripheral and central mechanisms of cough hypersensitivity.

作者信息

Singh Nabita, Driessen Alexandria K, McGovern Alice E, Moe Aung Aung Kywe, Farrell Michael J, Mazzone Stuart B

机构信息

Department of Medical Imaging and Radiation Sciences, Monash University, Clayton, Australia.

Department of Anatomy and Neuroscience, School of Biomedical Science, The University of Melbourne, Parkville, Australia.

出版信息

J Thorac Dis. 2020 Sep;12(9):5179-5193. doi: 10.21037/jtd-2020-icc-007.

DOI:10.21037/jtd-2020-icc-007
PMID:33145095
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7578480/
Abstract

Chronic cough is a difficult to treat symptom of many respiratory and some non-respiratory diseases, indicating that varied pathologies can underpin the development of chronic cough. However, clinically and experimentally it has been useful to collate these different pathological processes into the single unifying concept of cough hypersensitivity. Cough hypersensitivity syndrome is reflected by troublesome cough often precipitated by levels of stimuli that ordinarily don't cause cough in healthy people, and this appears to be a hallmark feature in many patients with chronic cough. Accordingly, a strong argument has emerged that changes in the excitability and/or normal regulation of the peripheral and central neural circuits responsible for cough are instrumental in establishing cough hypersensitivity and for causing excessive cough in disease. In this review, we explore the current peripheral and central neural mechanisms that are believed to be involved in altered cough sensitivity and present possible links to the mechanism of action of novel therapies that are currently undergoing clinical trials for chronic cough.

摘要

慢性咳嗽是许多呼吸道疾病和一些非呼吸道疾病难以治疗的症状,这表明多种病理状况可能是慢性咳嗽发生的基础。然而,在临床和实验中,将这些不同的病理过程归纳为咳嗽高敏这一统一概念是很有用的。咳嗽高敏综合征表现为通常不会在健康人身上引发咳嗽的刺激水平却常常诱发令人烦恼的咳嗽,而这似乎是许多慢性咳嗽患者的一个标志性特征。因此,一种有力的观点认为,负责咳嗽的外周和中枢神经回路的兴奋性和/或正常调节发生改变,在建立咳嗽高敏以及导致疾病中过度咳嗽方面起着重要作用。在本综述中,我们探讨了目前认为与咳嗽敏感性改变有关的外周和中枢神经机制,并介绍了与目前正在进行慢性咳嗽临床试验的新型疗法作用机制可能存在的联系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/343b/7578480/f26fb34c02c7/jtd-12-09-5179-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/343b/7578480/b1a6e5761ed5/jtd-12-09-5179-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/343b/7578480/0147c42d3e70/jtd-12-09-5179-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/343b/7578480/f26fb34c02c7/jtd-12-09-5179-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/343b/7578480/b1a6e5761ed5/jtd-12-09-5179-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/343b/7578480/0147c42d3e70/jtd-12-09-5179-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/343b/7578480/f26fb34c02c7/jtd-12-09-5179-f3.jpg

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Novel airway smooth muscle-mast cell interactions and a role for the TRPV4-ATP axis in non-atopic asthma.新型气道平滑肌-肥大细胞相互作用和 TRPV4-ATP 轴在非过敏性哮喘中的作用。
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