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本文引用的文献

1
Correctors promote folding of the CFTR in the endoplasmic reticulum.校正剂可促进囊性纤维化跨膜传导调节因子在内质网中的折叠。
Biochem J. 2008 Jul 1;413(1):29-36. doi: 10.1042/BJ20071690.
2
The DeltaF508-CFTR mutation results in increased biofilm formation by Pseudomonas aeruginosa by increasing iron availability.DeltaF508-CFTR突变通过增加铁的可利用性导致铜绿假单胞菌生物膜形成增加。
Am J Physiol Lung Cell Mol Physiol. 2008 Jul;295(1):L25-37. doi: 10.1152/ajplung.00391.2007. Epub 2008 Mar 21.
3
Enhanced cell-surface stability of rescued DeltaF508 cystic fibrosis transmembrane conductance regulator (CFTR) by pharmacological chaperones.通过药理伴侣增强挽救的ΔF508囊性纤维化跨膜传导调节因子（CFTR）的细胞表面稳定性。
Biochem J. 2008 Mar 15;410(3):555-64. doi: 10.1042/BJ20071420.
4
The Pseudomonas aeruginosa secreted protein PA2934 decreases apical membrane expression of the cystic fibrosis transmembrane conductance regulator.铜绿假单胞菌分泌蛋白PA2934可降低囊性纤维化跨膜传导调节因子的顶端膜表达。
Infect Immun. 2007 Aug;75(8):3902-12. doi: 10.1128/IAI.00338-07. Epub 2007 May 14.
5
MPB-07 reduces the inflammatory response to Pseudomonas aeruginosa in cystic fibrosis bronchial cells.MPB - 07可减轻囊性纤维化支气管细胞对铜绿假单胞菌的炎症反应。
Am J Respir Cell Mol Biol. 2007 May;36(5):615-24. doi: 10.1165/rcmb.2006-0200OC. Epub 2006 Dec 29.
6
Role of Ca2+ in responses of airway epithelia to Pseudomonas aeruginosa, flagellin, ATP, and thapsigargin.钙离子在气道上皮细胞对铜绿假单胞菌、鞭毛蛋白、三磷酸腺苷和毒胡萝卜素反应中的作用。
Am J Physiol Lung Cell Mol Physiol. 2007 Jan;292(1):L353-64. doi: 10.1152/ajplung.00042.2006. Epub 2006 Sep 8.
7
CFTR inhibition mimics the cystic fibrosis inflammatory profile.囊性纤维化跨膜传导调节因子（CFTR）抑制模拟了囊性纤维化的炎症特征。
Am J Physiol Lung Cell Mol Physiol. 2007 Feb;292(2):L383-95. doi: 10.1152/ajplung.00403.2005. Epub 2006 Aug 18.
8
Innate immune response in CF airway epithelia: hyperinflammatory?囊性纤维化气道上皮中的先天性免疫反应：炎症反应过度？
Am J Physiol Cell Physiol. 2006 Aug;291(2):C218-30. doi: 10.1152/ajpcell.00605.2005.
9
New insights into cystic fibrosis: molecular switches that regulate CFTR.囊性纤维化的新见解：调节囊性纤维化跨膜传导调节因子的分子开关
Nat Rev Mol Cell Biol. 2006 Jun;7(6):426-36. doi: 10.1038/nrm1949.
10
Dysregulated interleukin-8 secretion and NF-kappaB activity in human cystic fibrosis nasal epithelial cells.人囊性纤维化鼻上皮细胞中白细胞介素-8分泌失调与核因子-κB活性异常
J Cyst Fibros. 2006 May;5(2):113-9. doi: 10.1016/j.jcf.2005.12.003. Epub 2006 Feb 14.

Corr4A和VRT325不会降低人囊性纤维化气道上皮细胞对铜绿假单胞菌的炎症反应。

Corr4A and VRT325 do not reduce the inflammatory response to P. aeruginosa in human cystic fibrosis airway epithelial cells.

作者信息

Talebian Laleh, Coutermarsh Bonita, Channon Jacqueline Y, Stanton Bruce A

机构信息

Department of Physiology, Dartmouth Medical School, Hanover, Germany.

出版信息

Cell Physiol Biochem. 2009;23(1-3):199-204. doi: 10.1159/000204108. Epub 2009 Feb 18.

DOI:10.1159/000204108
PMID:19255514
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3711581/
Abstract

BACKGROUND

P. aeruginosa chronically colonizes the lung in CF patients and elicits a proinflammatory response. Excessive secretion of IL-6 and IL-8 by CF airway cells in response to P. aeruginosa infection in the CF airway is though to contribute to lung injury. Accordingly, the goal of this study was to test the hypothesis that Corr4a and VRT325, investigational compounds that increase DeltaF508-CFTR mediated Cl(-) secretion in human CF airway cells, reduce the pro-inflammatory response to P. aeruginosa.

METHODS

IL-6 and IL-8 secretion by polarized CF human airway epithelial cells (CFBE41o-) were measured by multiplex analysis, and DeltaF508-CFTR Cl- secretion was measured in Ussing chambers. Airway cells were exposed to P. aeruginosa (PAO1 or PA14) and Corr4a or VRT325.

RESULTS

Corr4a and VRT325 increased DeltaF508-CFTR Cl(-) secretion but did not reduce either constitutive IL-6 or IL-8 secretion, or IL-6 and IL-8 secretion stimulated by P. aeruginosa (PA14 or PAO1).

CONCLUSIONS

Corr4a and VRT325 do not reduce the inflammatory response to P. aeruginosa in human cystic fibrosis airway epithelial cells.

摘要

背景

铜绿假单胞菌长期定植于囊性纤维化（CF）患者的肺部并引发促炎反应。CF气道中的细胞因铜绿假单胞菌感染而过度分泌白细胞介素-6（IL-6）和白细胞介素-8（IL-8），这被认为会导致肺损伤。因此，本研究的目的是验证以下假设：Corr4a和VRT325（这两种研究性化合物可增加人CF气道细胞中DeltaF508-CFTR介导的氯离子分泌）可减轻对铜绿假单胞菌的促炎反应。

方法

通过多重分析测量极化的CF人气道上皮细胞（CFBE41o-）分泌IL-6和IL-8的情况，并在尤斯灌流小室中测量DeltaF508-CFTR氯离子分泌。将气道细胞暴露于铜绿假单胞菌（PAO1或PA14）以及Corr4a或VRT325中。

结果

Corr4a和VRT325增加了DeltaF508-CFTR氯离子分泌，但并未降低基础状态下IL-6或IL-8的分泌，也未降低由铜绿假单胞菌（PA14或PAO1）刺激引起的IL-6和IL-8分泌。

结论

Corr4a和VRT325不会减轻人囊性纤维化气道上皮细胞对铜绿假单胞菌的炎症反应。