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本文引用的文献

1
Impact of surfactant protein D, interleukin-5, and eosinophilia on Cryptococcosis.表面活性蛋白D、白细胞介素-5和嗜酸性粒细胞增多对隐球菌病的影响。
Infect Immun. 2014 Feb;82(2):683-93. doi: 10.1128/IAI.00855-13. Epub 2013 Nov 25.
2
Surfactant and allergic airway inflammation.表面活性物质与过敏性气道炎症。
Swiss Med Wkly. 2013 Jul 29;143:w13818. doi: 10.4414/smw.2013.13818. eCollection 2013.
3
Intriguing bronchoalveolar lavage proteome in a case of pulmonary langerhans cell histiocytosis.一例肺朗格汉斯细胞组织细胞增多症患者的有趣支气管肺泡灌洗蛋白质组
Am J Case Rep. 2013 Apr 29;14:129-33. doi: 10.12659/AJCR.889037. Print 2013.
4
Specific cleavage of the lung surfactant protein A by human cathepsin S may impair its antibacterial properties.人组织蛋白酶 S 对肺表面活性蛋白 A 的特异性切割可能会损害其抗菌特性。
Int J Biochem Cell Biol. 2013 Aug;45(8):1701-9. doi: 10.1016/j.biocel.2013.05.018. Epub 2013 May 22.
5
Protective effects of exogenous surfactant protein A in allergic rhinitis: a mouse model.外源性表面活性蛋白A在变应性鼻炎中的保护作用:小鼠模型
Ann Otol Rhinol Laryngol. 2013 Apr;122(4):240-6. doi: 10.1177/000348941312200405.
6
Predicting sputum eosinophilia in exacerbations of COPD using exhaled nitric oxide.利用呼出气一氧化氮预测 COPD 加重期痰液中嗜酸性粒细胞增多。
Inflammation. 2013 Oct;36(5):1178-85. doi: 10.1007/s10753-013-9653-8.
7
Surfactant protein-A modulates LPS-induced TLR4 localization and signaling via β-arrestin 2.表面活性蛋白 A 通过β-arrestin 2 调节脂多糖诱导的 TLR4 定位和信号转导。
PLoS One. 2013;8(3):e59896. doi: 10.1371/journal.pone.0059896. Epub 2013 Mar 25.
8
A TLR4-interacting SPA4 peptide inhibits LPS-induced lung inflammation.TLR4 相互作用的 SPA4 肽抑制 LPS 诱导的肺部炎症。
Innate Immun. 2013 Dec;19(6):596-610. doi: 10.1177/1753425912474851. Epub 2013 Mar 8.
9
Detection of surfactant proteins A, B, C, and D in human nasal mucosa and their regulation in chronic rhinosinusitis with polyps.检测人鼻黏膜中的表面活性剂蛋白 A、B、C 和 D 及其在鼻息肉慢性鼻窦炎中的调控作用。
Am J Rhinol Allergy. 2013 Jan;27(1):24-9. doi: 10.2500/ajra.2013.27.3838.
10
NET balancing: a problem in inflammatory lung diseases.网络平衡:炎症性肺疾病的一个问题。
Front Immunol. 2013 Jan 24;4:1. doi: 10.3389/fimmu.2013.00001. eCollection 2013.

嗜酸粒细胞相关肺部疾病。表面活性蛋白 A 和 D 的帮助呼之欲出?

Eosinophil-associated lung diseases. A cry for surfactant proteins A and D help?

机构信息

1 Department of Medicine, Division of Pulmonary, Allergy and Critical Care, and.

出版信息

Am J Respir Cell Mol Biol. 2014 Nov;51(5):604-14. doi: 10.1165/rcmb.2014-0095TR.

DOI:10.1165/rcmb.2014-0095TR
PMID:24960334
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4224083/
Abstract

Surfactant proteins (SP)-A and SP-D (SP-A/-D) play important roles in numerous eosinophil-dominated diseases, including asthma, allergic bronchopulmonary aspergillosis, and allergic rhinitis. In these settings, SP-A/-D have been shown to modulate eosinophil chemotaxis, inhibit eosinophil mediator release, and mediate macrophage clearance of apoptotic eosinophils. Dysregulation of SP-A/-D function in eosinophil-dominated diseases is also not uncommon. Alterations in serum SP-A/-D levels are associated with disease severity in allergic rhinitis and chronic obstructive pulmonary disease. Furthermore, oligimerization of SP-A/-D, necessary for their proper function, can be perturbed by reactive nitrogen species, which are increased in eosinophilic disease. In this review, we highlight the associations of eosinophilic lung diseases with SP-A and SP-D levels and functions.

摘要

表面活性蛋白(SP)-A 和 SP-D(SP-A/-D)在许多嗜酸性粒细胞主导的疾病中发挥重要作用,包括哮喘、变应性支气管肺曲霉病和变应性鼻炎。在这些情况下,已经表明 SP-A/-D 可以调节嗜酸性粒细胞趋化性、抑制嗜酸性粒细胞介质释放,并介导巨噬细胞清除凋亡的嗜酸性粒细胞。在嗜酸性粒细胞主导的疾病中,SP-A/-D 功能的失调也并不罕见。血清 SP-A/-D 水平的改变与变应性鼻炎和慢性阻塞性肺疾病的疾病严重程度相关。此外,SP-A/-D 的寡聚化对于其正常功能是必要的,但可被反应性氮物种破坏,而这些物质在嗜酸性粒细胞疾病中增加。在这篇综述中,我们强调了嗜酸性粒细胞性肺病与 SP-A 和 SP-D 水平和功能的关联。