scholarly journals 55 Tight junction regulation and AAV-2 mediated gene transfer in a cystic fibrosis airway epithelial cell line

2005 ◽  
Vol 4 ◽  
pp. S16
Keyword(s):  
Cystic Fibrosis ◽  
Gene Transfer ◽  
Epithelial Cell ◽  
Tight Junction ◽  
Cell Line ◽  
Airway Epithelial Cell ◽  
Epithelial Cell Line ◽  
Airway Epithelial ◽  
Cystic Fibrosis Airway ◽  
Tight Junction Regulation

scholarly journals Prostasin, a membrane-anchored serine peptidase, regulates sodium currents in JME/CF15 cells, a cystic fibrosis airway epithelial cell line

2004 ◽  
Vol 287 (5) ◽  
pp. L928-L935 ◽  
Author(s):  
Zhenyue Tong ◽  
Beate Illek ◽  
Vikash J. Bhagwandin ◽  
George M. Verghese ◽  
George H. Caughey
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Airway Epithelial Cell ◽  
Epithelial Cell Line ◽  
Airway Epithelial ◽  
Ussing Chambers ◽  
Serine Peptidase ◽  
Cystic Fibrosis Airway ◽  
Interfering Rna

Prostasin is a tryptic peptidase expressed in prostate, kidney, lung, and airway. Mammalian prostasins are related to Xenopus channel-activating protease, which stimulates epithelial Na+ channel (ENaC) activity in frogs. In human epithelia, prostasin is one of several membrane peptidases proposed to regulate ENaC. This study tests the hypothesis that prostasin can regulate ENaC in cystic fibrosis epithelia in which excessive Na+ uptake contributes to salt and water imbalance. We show that prostasin mRNA and protein are strongly expressed by human airway epithelial cell lines, including immortalized JME/CF15 nasal epithelial cells homozygous for the ΔF508 cystic fibrosis mutation. Epithelial cells transfected with vectors encoding recombinant soluble prostasin secrete active, tryptic peptidase that is highly sensitive to inactivation by aprotinin. When studied as monolayers in Ussing chambers, JME/CF15 cells exhibit amiloride-sensitive, transepithelial Na+ currents that are markedly diminished by aprotinin, suggesting regulation by serine-class peptidases. Overproduction of membrane-anchored prostasin in transfected JME/CF15 cells does not augment Na+ currents, and trypsin-induced increases are small, suggesting that baseline serine peptidase-dependent ENaC activation is maximal in these cells. To probe prostasin’s involvement in basal ENaC activity, we silenced expression of prostasin using short interfering RNA targeting of prostasin mRNA’s 3′-untranslated region. This drops ENaC currents to 26 ± 9% of baseline. These data predict that prostasin is a major regulator of ENaC-mediated Na+ current in ΔF508 cystic fibrosis epithelia and suggest that airway prostasin is a target for therapeutic inhibition to normalize ion current in cystic fibrosis airway.

scholarly journals Stimulation of chloride secretion by P1 purinoceptor agonists in cystic fibrosis phenotype airway epithelial cell line CFPEo-

1994 ◽  
Vol 112 (1) ◽  
pp. 169-175 ◽  
Author(s):  
Anthony C. Chao ◽  
Jonathan B. Zifferblatt ◽  
John A. Wagner ◽  
Y.-J. Dong ◽  
Dieter C. Gruenert ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cell ◽  
Cell Line ◽  
Airway Epithelial Cell ◽  
Chloride Secretion ◽  
Epithelial Cell Line ◽  
Airway Epithelial ◽  
Stimulation Of

Prostaglandin E2-induced interleukin-6 release by a human airway epithelial cell line

2001 ◽  
Vol 280 (1) ◽  
pp. L127-L133 ◽  
Author(s):  
S. Tavakoli ◽  
M. J. Cowan ◽  
T. Benfield ◽  
C. Logun ◽  
J. H. Shelhamer
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Airway Epithelial Cell ◽  
Epithelial Cell Line ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cell ◽  
Cell Release

Human airway epithelial cell release of interleukin (IL)-6 in response to lipid mediators was studied in an airway cell line (BEAS-2B). Prostaglandin (PG) E2(10−7M) treatment caused an increase in IL-6 release at 2, 4, 8, and 24 h. IL-6 release into the culture medium at 24 h was 3,396 ± 306 vs. 1,051 ± 154 pg/ml (PGE2-treated cells vs. control cells). PGE2(10−7to 10−10M) induced a dose-related increase in IL-6 release at 24 h. PGF2α(10−6M) treatment caused a similar effect to that of PGE2(10−7M). PGE2analogs with relative selectivity for PGE2receptor subtypes were studied. Sulprostone, a selective agonist for the EP-3 receptor subtype had no effect on IL-6 release. 11-Deoxy-16,16-dimethyl-PGE2, an EP-2/4 agonist, and 17-phenyl trinor PGE2, an agonist selective for the EP-1 > EP-3 receptor subtype (10−6to 10−8M), caused dose-dependent increases in IL-6 release. 8-Bromo-cAMP treatment resulted in dose-related increases in IL-6 release. RT-PCR of BEAS-2B cell mRNA demonstrated mRNA for EP-1, EP-2, and EP-4 receptors. After PGE2treatment, increases in IL-6 mRNA were noted at 4 and 18 h. Therefore, PGE2increases airway epithelial cell IL-6 production and release.

RSV infection of the airway epithelial cell line BEAS-2B stimulate NK cells

2017 ◽  
Author(s):  
Jennifer Davies ◽  
Rachel Corkhill ◽  
Steve Christmas ◽  
Paul McNamara ◽  
Brian Flanagan
Keyword(s):  
Epithelial Cell ◽  
Nk Cells ◽  
Cell Line ◽  
Airway Epithelial Cell ◽  
Epithelial Cell Line ◽  
Airway Epithelial ◽  
Rsv Infection
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