Interaction of an artificial surfactant in human pulmonary epithelial cells

2005 ◽  
Vol 39 (2) ◽  
pp. 167-177 ◽  
Author(s):  
Edgar J. Romero ◽  
Fernando R. Moya ◽  
Michael J. Tuvim ◽  
Joseph L. Alcorn
Keyword(s):  
Epithelial Cells ◽  
Pulmonary Epithelial Cells ◽  
Artificial Surfactant

scholarly journals Long-Term Exposure to Nanosized TiO2 Triggers Stress Responses and Cell Death Pathways in Pulmonary Epithelial Cells

2021 ◽  
Vol 22 (10) ◽  
pp. 5349
Author(s):  
Mayes Alswady-Hoff ◽  
Johanna Samulin Erdem ◽  
Santosh Phuyal ◽  
Oskar Knittelfelder ◽  
Animesh Sharma ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Health Effects ◽  
Stress Responses ◽  
Cell Stress ◽  
Lipid Classes ◽  
Long Term Effects ◽  
Cell Death Pathways ◽  
Pulmonary Epithelial Cells

There is little in vitro data available on long-term effects of TiO2 exposure. Such data are important for improving the understanding of underlying mechanisms of adverse health effects of TiO2. Here, we exposed pulmonary epithelial cells to two doses (0.96 and 1.92 µg/cm2) of TiO2 for 13 weeks and effects on cell cycle and cell death mechanisms, i.e., apoptosis and autophagy were determined after 4, 8 and 13 weeks of exposure. Changes in telomere length, cellular protein levels and lipid classes were also analyzed at 13 weeks of exposure. We observed that the TiO2 exposure increased the fraction of cells in G1-phase and reduced the fraction of cells in G2-phase, which was accompanied by an increase in the fraction of late apoptotic/necrotic cells. This corresponded with an induced expression of key apoptotic proteins i.e., BAD and BAX, and an accumulation of several lipid classes involved in cellular stress and apoptosis. These findings were further supported by quantitative proteome profiling data showing an increase in proteins involved in cell stress and genomic maintenance pathways following TiO2 exposure. Altogether, we suggest that cell stress response and cell death pathways may be important molecular events in long-term health effects of TiO2.

Effects of alpha particle radiation on gene expression in human pulmonary epithelial cells

2012 ◽  
Vol 215 (5) ◽  
pp. 522-535 ◽  
Author(s):  
Vinita Chauhan ◽  
Matthew Howland ◽  
Amy Mendenhall ◽  
Shifawn O’Hara ◽  
Trevor J. Stocki ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Alpha Particle ◽  
Particle Radiation ◽  
Pulmonary Epithelial Cells

Actin-Containing Microfilaments of Pulmonary Epithelial Cells Provide a Mechanism for Translocating Asbestos to the Interstitium

CHEST Journal ◽  
1983 ◽  
Vol 83 (5) ◽  
pp. 11S-12S ◽  
Author(s):  
Arnold R. Brody ◽  
Lila H. Hill ◽  
William S. Stirewalt ◽  
Kenneth B. Adler
Keyword(s):  
Epithelial Cells ◽  
Pulmonary Epithelial Cells

scholarly journals Phosphocholine-Modified Lipooligosaccharides of Haemophilus influenzae Inhibit ATP-Induced IL-1β Release by Pulmonary Epithelial Cells

Molecules ◽  
2018 ◽  
Vol 23 (8) ◽  
pp. 1979 ◽  
Author(s):  
Katrin Richter ◽  
Christian Koch ◽  
Alexander Perniss ◽  
Philipp Wolf ◽  
Elke Schweda ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Haemophilus Influenzae ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Opportunistic Pathogen ◽  
Mammalian Host ◽  
Nicotinic Acetylcholine ◽  
Pulmonary Epithelial Cells ◽  
Airway Infections ◽  
Human Lung Carcinoma

Phosphocholine-modified bacterial cell wall components are virulence factors enabling immune evasion and permanent colonization of the mammalian host, by mechanisms that are poorly understood. Recently, we demonstrated that free phosphocholine (PC) and PC-modified lipooligosaccharides (PC-LOS) from Haemophilus influenzae, an opportunistic pathogen of the upper and lower airways, function as unconventional nicotinic agonists and efficiently inhibit the ATP-induced release of monocytic IL-1β. We hypothesize that H. influenzae PC-LOS exert similar effects on pulmonary epithelial cells and on the complex lung tissue. The human lung carcinoma-derived epithelial cell lines A549 and Calu-3 were primed with lipopolysaccharide from Escherichia coli followed by stimulation with ATP in the presence or absence of PC or PC-LOS or LOS devoid of PC. The involvement of nicotinic acetylcholine receptors was tested using specific antagonists. We demonstrate that PC and PC-LOS efficiently inhibit ATP-mediated IL-1β release by A549 and Calu-3 cells via nicotinic acetylcholine receptors containing subunits α7, α9, and/or α10. Primed precision-cut lung slices behaved similarly. We conclude that H. influenzae hijacked an endogenous anti-inflammatory cholinergic control mechanism of the lung to evade innate immune responses of the host. These findings may pave the way towards a host-centered antibiotic treatment of chronic airway infections with H. influenzae.

Cigarette Smoke Suppresses PPAR-γ Expression and Activation In Murine Pulmonary Epithelial Cells

2012 ◽  
Vol 9 (2) ◽  
pp. 82-82
Author(s):  
Sandra M. Wells ◽  
Jason Weigel ◽  
Fengxia Xiao ◽  
Elizabeth B. Klein
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Ppar Γ ◽  
Pulmonary Epithelial Cells
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