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宿主细胞受体表达上调是否为细菌黏附与慢性呼吸道疾病之间提供了一种联系?

Does upregulated host cell receptor expression provide a link between bacterial adhesion and chronic respiratory disease?

作者信息

O'Toole Ronan F, Shukla Shakti D, Walters Eugene H

机构信息

School of Medicine, Faculty of Health, University of Tasmania, Medical Science 1, 17 Liverpool Street, Hobart, TAS, 7000, Australia.

出版信息

J Transl Med. 2016 Oct 26;14(1):304. doi: 10.1186/s12967-016-1063-x.

DOI:10.1186/s12967-016-1063-x
PMID:27782846
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5080759/
Abstract

Expression of the platelet-activating factor receptor is upregulated in the respiratory epithelium of smokers and chronic obstructive pulmonary disease patients. We have recently determined that increased expression of PAFr correlates with higher levels of adhesion to human bronchial epithelial cells by non-typable Haemophilus influenzae and Streptococcus pneumoniae which are major bacterial pathogens in acute exacerbations of COPD. In addition, we found that a PAFr antagonist decreased the adhesion of both respiratory bacterial pathogens to non-cigarette exposure control levels. This highlights the possibility that epithelial receptors, that are upregulated in response to cigarette smoke, could be targeted to specifically block chronic bacterial infections of the lower respiratory tract. In this commentary, we explore the question of whether adhesion to a temporally-upregulated host receptor is a common event in chronic bacterial disease, and as such, could represent a putative therapeutic target for blocking infection by respiratory and other pathogens.

摘要

血小板活化因子受体在吸烟者和慢性阻塞性肺疾病患者的呼吸道上皮中表达上调。我们最近确定,PAFr表达增加与不可分型流感嗜血杆菌和肺炎链球菌对人支气管上皮细胞的粘附水平升高相关,这两种细菌是慢性阻塞性肺疾病急性加重期的主要病原菌。此外,我们发现PAFr拮抗剂可将两种呼吸道病原菌的粘附降低至非香烟暴露对照水平。这突出了一种可能性,即响应香烟烟雾而上调的上皮受体可能成为特异性阻断下呼吸道慢性细菌感染的靶点。在这篇评论中,我们探讨了粘附于暂时上调的宿主受体是否是慢性细菌性疾病中的常见现象,以及是否因此可能成为阻断呼吸道和其他病原体感染的潜在治疗靶点这一问题。

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本文引用的文献

1
An antagonist of the platelet-activating factor receptor inhibits adherence of both nontypeable Haemophilus influenzae and Streptococcus pneumoniae to cultured human bronchial epithelial cells exposed to cigarette smoke.血小板活化因子受体拮抗剂可抑制不可分型流感嗜血杆菌和肺炎链球菌对暴露于香烟烟雾中的培养人支气管上皮细胞的黏附。
Int J Chron Obstruct Pulmon Dis. 2016 Jul 25;11:1647-55. doi: 10.2147/COPD.S108698. eCollection 2016.
2
Platelet-activating factor receptor (PAFr) is upregulated in small airways and alveoli of smokers and COPD patients.血小板活化因子受体(PAFr)在吸烟者和慢性阻塞性肺疾病(COPD)患者的小气道和肺泡中上调。
Respirology. 2016 Apr;21(3):504-10. doi: 10.1111/resp.12709. Epub 2015 Dec 10.
3
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4
Influenza viral neuraminidase primes bacterial coinfection through TGF-β-mediated expression of host cell receptors.流感病毒神经氨酸酶通过转化生长因子-β介导的宿主细胞受体表达引发细菌共感染。
Proc Natl Acad Sci U S A. 2015 Jan 6;112(1):238-43. doi: 10.1073/pnas.1414422112. Epub 2014 Dec 22.
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