scholarly journals In vitro evaluation of tobramycin and aztreonam versus Pseudomonas aeruginosa biofilms on cystic fibrosis-derived human airway epithelial cells

2012 ◽  
Vol 67 (11) ◽  
pp. 2673-2681 ◽  
Author(s):  
Q. Yu ◽  
E. F. Griffin ◽  
S. Moreau-Marquis ◽  
J. D. Schwartzman ◽  
B. A. Stanton ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
In Vitro Evaluation ◽  
Human Airway ◽  
Human Airway Epithelial Cells

In vitro evaluation of the toxicity induced by nickel soluble and particulate forms in human airway epithelial cells

2011 ◽  
Vol 25 (2) ◽  
pp. 454-461 ◽  
Author(s):  
Efrat Forti ◽  
Susan Salovaara ◽  
Yuksel Cetin ◽  
Anna Bulgheroni ◽  
Richard Tessadri ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
In Vitro Evaluation ◽  
Human Airway ◽  
Human Airway Epithelial Cells

G protein G alpha i-2 inhibits outwardly rectifying chloride channels in human airway epithelial cells

1995 ◽  
Vol 269 (2) ◽  
pp. C451-C456 ◽  
Author(s):  
E. M. Schwiebert ◽  
D. C. Gruenert ◽  
W. B. Guggino ◽  
B. A. Stanton
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
G Protein ◽  
G Proteins ◽  
Airway Epithelial Cells ◽  
Protein G ◽  
Airway Epithelial ◽  
Human Airway ◽  
Cl Channels ◽  
Human Airway Epithelial Cells

Previously we demonstrated that the heterotrimeric G protein, G alpha i-2, inhibits cystic fibrosis transmembrane conductance regulator (CFTR) chloride (Cl-) channels in human airway epithelial cells (E. M. Schwiebert, F. Gesek, L. Ercolani, C. Wjasow, D. C. Gruenert, and B. A. Stanton. Am. J. Physiol. 267 (Cell Physiol. 36): C272-C281, 1994, and E. M. Schwiebert, N. L. Kizer, D. C. Gruenert, and B. A. Stanton. Proc. Natl. Acad. Sci. USA 89: 10623-10627, 1992). The goal of the present study was to determine if G proteins also regulate outwardly rectifying Cl- channels (ORCC), a distinct class of Cl- channels regulated defectively by protein kinase A (PKA) in cystic fibrosis (CF). To this end, we used the patch-clamp technique to study ORCC in a normal human airway epithelial cell line (9HTEo-) that expresses CFTR and ORCC. Stimulation of G proteins with GTP and GTP gamma S decreased the single-channel open probability (Po) of ORCC, whereas inhibition of G proteins by GDP beta S increased the Po. Moreover, pertussis toxin (PTX), an uncoupler of Gi and G(o) subclasses of heterotrimeric G proteins, also increased the Po. Purified G alpha i-2 decreased the Po. In contrast, other PTX-sensitive G proteins, G alpha i-1, G alpha i-3, and G alpha o, had no effect on Po. We propose that G alpha i-2 couples to a receptor whose agonist negatively regulates ORCC in human airway epithelial cells.

Ozone-induced release of cytokines and fibronectin by alveolar macrophages and airway epithelial cells

1994 ◽  
Vol 266 (6) ◽  
pp. L612-L619 ◽  
Author(s):  
R. B. Devlin ◽  
K. P. McKinnon ◽  
T. Noah ◽  
S. Becker ◽  
H. S. Koren
Keyword(s):  
Epithelial Cells ◽  
Cell Line ◽  
Alveolar Macrophages ◽  
Airway Epithelial Cells ◽  
Airway Hyperreactivity ◽  
Ozone Exposure ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cells

Acute exposure of animals and humans to ozone results in decrements in lung function, development of airway hyperreactivity, inflammation, edema, damage to pulmonary cells, and production of several compounds with tissue damaging, fibrinogenic or fibrotic potential. The contribution of airway epithelial cells and alveolar macrophages to these processes is unclear. In this study we have directly exposed human alveolar macrophages and human airway epithelial cells to ozone in vitro and measured the cytotoxic effects of ozone, as well as the production of the inflammatory cytokines interleukin-6 (IL-6) and interleukin-8 (IL-8), and fibronectin, all of which are substantially elevated in the bronchoalveolar lavage fluid of humans exposed to ozone. Cells were grown on rigid, collagen-impregnated filter supports, and the interaction of cells with ozone facilitated by exposing them to the gas with medium below the support but no medium on top of the cells. The results show that, although macrophages are much more sensitive to ozone than epithelial cells, they do not produce increased amounts of IL-6, IL-8, or fibronectin following ozone exposure. In contrast, epithelial cells produce substantially more of all three proteins following ozone exposure, and both IL-6 and fibronectin are secreted vectorially. An immortalized human airway epithelial cell line (BEAS 2B) was used in these experiments since human airway epithelial cells are infrequently available for in vitro studies. Data from this study extend previous findings which suggest that the BEAS cell line is a useful model to study the interaction between airway epithelial cells and environmental toxicants.

Alpha 1-adrenergic signaling in human airway epithelial cells involves inositol lipid and phosphate metabolism

1992 ◽  
Vol 262 (2) ◽  
pp. L183-L191 ◽  
Author(s):  
C. M. Liedtke
Keyword(s):  
Epithelial Cells ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Nasal Epithelial Cells ◽  
Human Airway ◽  
Adrenergic Antagonist ◽  
Human Airway Epithelial Cells

A role for phospholipase C (PLC) hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) as a mechanism of alpha 1-adrenergic signal transduction in human airway epithelial cells (AEC) was investigated in isolated normal tracheal and cystic fibrosis (CF) nasal epithelial cells grown in in vitro culture and prelabeled with 3 muCi myo-[3H]inositol/ml for 72 h. Breakdown of polyphosphoinositides was measured using thin-layer chromatography to detect phosphatidylinositol, phosphatidylinositol 4-phosphate (PIP), and PIP2. Inositol phosphates were separated by ion-exchange column chromatography. In normal AEC, the addition of the endogenous catecholamine l-epinephrine produced a rapid, transient accumulation of inositol 1,4,5-trisphosphate (IP3) and inositol 1,4-bisphosphate (IP2) and breakdown of PIP and PIP2. IP3 increased 1.7-fold and IP2 1.6-fold after 20 and 40 s, respectively. A maximal decrease of 35% PIP2 and 30% PIP is observed after 20 and 40 s, respectively. The effects of l-epinephrine were not blocked by the beta-adrenergic antagonist dl-propranolol but were mimicked by the alpha 1-adrenergic agonist methoxamine. Prazosin, an alpha 1-adrenergic antagonist, and pertussis toxin (PTX) blocked the effects of l-epinephrine and methoxamine. Addition of l-epinephrine and methoxamine to CF nasal epithelial cells also induced prazosin-sensitive polyphosphoinositide breakdown and inositol phosphate accumulation. A 2.2-fold accumulation of IP3 was observed after 10 s and 2.0-fold increase in IP2 after 20 s. Maximal decreases of 32% PIP2 and 23% PIP levels were observed after 20-s incubation with l-epinephrine. PTX reduced the effects of l-epinephrine and significantly blocked the effects of methoxamine.(ABSTRACT TRUNCATED AT 250 WORDS)

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