scholarly journals Effect of long-acting β-agonists/glucocorticoids on human airway epithelial cell cytokine, transcriptomic and oxidative stress responses to cannabis smoke

2020 ◽  
Vol 6 (1) ◽  
pp. 00265-2019 ◽  
Author(s):  
Ryan D. Huff ◽  
Jennifer A. Aguiar ◽  
Wayne Tse ◽  
Martin R. Stämpfli ◽  
Brendan J. McConkey ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
Stress Responses ◽  
Airway Epithelial Cell ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cell ◽  
Long Acting ◽  
Oxidative Stress Responses ◽  
And Oxidative Stress

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.

scholarly journals Human airway epithelial cell culture to identify new respiratory viruses: Coronavirus NL63 as a model

2009 ◽  
Vol 156 (1-2) ◽  
pp. 19-26 ◽  
Author(s):  
Bridget S. Banach ◽  
Jan M. Orenstein ◽  
Linda M. Fox ◽  
Scott H. Randell ◽  
Anne H. Rowley ◽  
...  
Keyword(s):  
Cell Culture ◽  
Epithelial Cell ◽  
Airway Epithelial Cell ◽  
Respiratory Viruses ◽  
Airway Epithelial ◽  
Epithelial Cell Culture ◽  
Human Airway ◽  
Human Airway Epithelial Cell

15-Deoxy-Δ12,14-Prostaglandin J2 Induces IL-8 and GM-CSF in a Human Airway Epithelial Cell Line (NCI-H292)

2009 ◽  
Vol 149 (1) ◽  
pp. 77-82 ◽  
Author(s):  
Takahito Chiba ◽  
Shigeharu Ueki ◽  
Wataru Ito ◽  
Hikari Kato ◽  
Masahide Takeda ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Airway Epithelial Cell ◽  
Epithelial Cell Line ◽  
Airway Epithelial ◽  
Gm Csf ◽  
Human Airway ◽  
Human Airway Epithelial Cell

scholarly journals Purinergic signaling underlies CFTR control of human airway epithelial cell volume

2004 ◽  
Vol 3 (2) ◽  
pp. 99-117 ◽  
Author(s):  
Gavin M Braunstein ◽  
Akos Zsembery ◽  
Torry A Tucker ◽  
Erik M Schwiebert
Keyword(s):  
Epithelial Cell ◽  
Cell Volume ◽  
Airway Epithelial Cell ◽  
Purinergic Signaling ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cell

scholarly journals Identification of a Human Airway Epithelial Cell Subpopulation with Altered Biophysical, Molecular, and Metastatic Properties

2017 ◽  
Vol 10 (9) ◽  
pp. 514-524 ◽  
Author(s):  
Paul C. Pagano ◽  
Linh M. Tran ◽  
Nawal Bendris ◽  
Sean O'Byrne ◽  
Henry T. Tse ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Airway Epithelial Cell ◽  
Cell Subpopulation ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cell

scholarly journals A novel approach to analyze gene expression data demonstrates that the ΔF508 mutation in CFTR downregulates the antigen presentation pathway

2010 ◽  
Vol 298 (4) ◽  
pp. L473-L482 ◽  
Author(s):  
Thomas H. Hampton ◽  
Bruce A. Stanton
Keyword(s):  
Gene Expression ◽  
Epithelial Cell ◽  
Immune Function ◽  
Antigen Presentation ◽  
Mhc Class I ◽  
Airway Epithelial Cell ◽  
Class I ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cell

Gene array studies comparing cystic fibrosis (CF) and non-CF genotypes should reveal factors that explain variability in CF lung disease progression, yielding insights that lead to improved CF care. To date, studies have reached conflicting conclusions, perhaps due to experimental differences and divergent statistical approaches. This review aims: 1) to summarize the findings of four recent gene studies comparing CF and non-CF genotypes, and 2) to reanalyze original data using a recently developed statistical approach, with the aim of identifying genes and paths consistently regulated by the CF genotype. We identified four studies evaluating the effect of the ΔF508-CFTR mutation on human airway epithelial cell gene expression, restricting our investigation to human airway epithelial cell studies whose data were accessible in NCBI's Gene Expression Omnibus or the European Bioinformatic Institute's ArrayExpress. Gene expression patterns showed consistent repression of MHC class I antigen presentation genes in CF human airway epithelia, suggesting a novel mechanistic explanation for poor clearance of viral and bacterial infections by CF patients. We also examined proinflammatory and NF-κB genes, whose induction is widely accepted as a hallmark of the CF genotype, but found little evidence of induction, consistent with a recent review (Machen TE, Am J Physiol Cell Physiol 291: C218–C230, 2006.). In conclusion, our analysis suggests that the CF genotype may impair immune function in airway epithelial cells but may not increase inflammation. Additional studies are required to determine whether MHC class I gene repression in CF reduces antigen presentation at the protein level and whether repression impairs immune function.

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