Neuroimmune Pathophysiology in Asthma.
Neuroimmune Pathophysiology in Asthma.
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哮喘的神经免疫病理生理学。
DOI：
10.3389/fcell.2021.663535
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发表时间：
2021
影响因子：
5.5
通讯作者：
Terán LM
中科院分区：
文献类型：
--
作者：
Pavón-Romero GF;Serrano-Pérez NH;García-Sánchez L;Ramírez-Jiménez F;Terán LM
哮喘是一种以支气管高反应性为特征的慢性下气道炎症性疾病。I型超敏反应是包括过敏性哮喘在内的所有特应性疾病的基础。然而，与炎症机制相比，神经递质（NT）和神经肽（NP）在这种疾病中的作用较少被探索。事实上，气道上皮含有充满神经递质（5-羟色胺和GABA）和神经肽（P物质[SP]、神经激肽A [NKA]、血管活性肠肽[VIP]、降钙素基因相关肽[CGRP]和降钙素-[N/OFQ]）的肺神经内分泌细胞，这些神经递质和神经肽在过敏原暴露后释放。同样，自主气道纤维产生乙酰胆碱（ACh）和神经肽Y（NPY）。这些NT/NP的作用不同; SP、NKA和5-羟色胺发挥促炎作用，而VIP、N/OFQ和GABA显示抗炎活性。然而，CGPR和ACh具有双重作用。例如，ACh-M3轴诱导杯状细胞化生、细胞外基质沉积和支气管收缩; CGRP-RAMP 1轴增强Th 2和Th 9应答; SP-NK 1 R轴促进嗜酸性粒细胞、肥大细胞和中性粒细胞中趋化因子的合成。相比之下，ILC 2中的ACh-α 7 nAChR轴减少了TNF-α、IL-1和IL-6的合成，从而减轻肺部炎症，而VIP-VPAC 1、N/OFQ-NOP轴则引起支气管扩张和抗炎作用。某些NT/NP如5-HT、NKA可作为哮喘患者的生物标志物。事实上，基于吸入皮质类固醇和抗胆碱能药物的哮喘治疗阻断了M3和TRPV 1受体。此外，实验性药物如NK 1 R/NK 2 R拮抗剂和外源性VIP的给药降低了炎症介质，表明调节NT/NP的作用代表了治疗哮喘的潜在新方法。
Asthma is a chronic inflammation of lower airway disease, characterized by bronchial hyperresponsiveness. Type I hypersensitivity underlies all atopic diseases including allergic asthma. However, the role of neurotransmitters (NT) and neuropeptides (NP) in this disease has been less explored in comparison with inflammatory mechanisms. Indeed, the airway epithelium contains pulmonary neuroendocrine cells filled with neurotransmitters (serotonin and GABA) and neuropeptides (substance P[SP], neurokinin A [NKA], vasoactive intestinal peptide [VIP], Calcitonin-gene related peptide [CGRP], and orphanins-[N/OFQ]), which are released after allergen exposure. Likewise, the autonomic airway fibers produce acetylcholine (ACh) and the neuropeptide Y(NPY). These NT/NP differ in their effects; SP, NKA, and serotonin exert pro-inflammatory effects, whereas VIP, N/OFQ, and GABA show anti-inflammatory activity. However, CGPR and ACh have dual effects. For example, the ACh-M3 axis induces goblet cell metaplasia, extracellular matrix deposition, and bronchoconstriction; the CGRP-RAMP1 axis enhances Th2 and Th9 responses; and the SP-NK1R axis promotes the synthesis of chemokines in eosinophils, mast cells, and neutrophils. In contrast, the ACh-α7nAChR axis in ILC2 diminishes the synthesis of TNF-α, IL-1, and IL-6, attenuating lung inflammation whereas, VIP-VPAC1, N/OFQ-NOP axes cause bronchodilation and anti-inflammatory effects. Some NT/NP as 5-HT and NKA could be used as biomarkers to monitor asthma patients. In fact, the asthma treatment based on inhaled corticosteroids and anticholinergics blocks M3 and TRPV1 receptors. Moreover, the administration of experimental agents such as NK1R/NK2R antagonists and exogenous VIP decrease inflammatory mediators, suggesting that regulating the effects of NT/NP represents a potential novel approach for the treatment of asthma.
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影响因子：
24.3
作者：
Bos, I. S. T.;Gosens, R.;Zaagsma, J.
通讯作者：
Zaagsma, J.
影响因子：
14.2
作者：
Bonner, Kandace;Kariyawasam, Harsha H.;Kay, A. Barry
通讯作者：
Kay, A. Barry
影响因子：
7.3
作者：
BRAIN, SD;WILLIAMS, TJ
通讯作者：
WILLIAMS, TJ
影响因子：
3.4
作者：
Caberlotto, L;Hurd, YL;Carletti, R
通讯作者：
Carletti, R
DOI：
10.1165/rcmb.2018-0179oc
发表时间：
2019-06-01
影响因子：
6.4
作者：
Barrios, Juliana;Kho, Alvin T.;Ai, Xingbin
通讯作者：
Ai, Xingbin