scholarly journals Effects of hydrogen peroxide on mucociliary transport in human airway epithelial cells

2014 ◽  
Vol 24 (3) ◽  
pp. 191-195 ◽  
Author(s):  
Akiko Honda ◽  
Rumiko Murayama ◽  
Yugo Matsuda ◽  
Kenshi Tsuji ◽  
Takahiro Sawahara ◽  
...  
2011 ◽  
Vol 37 (10) ◽  
pp. 606-614 ◽  
Author(s):  
JeanClare Seagrave ◽  
Helmut Albrecht ◽  
Yong Sung Park ◽  
Bruce Rubin ◽  
Gail Solomon ◽  
...  

2015 ◽  
Vol 309 (2) ◽  
pp. L99-L108 ◽  
Author(s):  
Patrick R. Sears ◽  
Wei-Ning Yin ◽  
Lawrence E. Ostrowski

Mucociliary clearance (MCC) is an important innate defense mechanism that continuously removes inhaled pathogens and particulates from the airways. Normal MCC is essential for maintaining a healthy respiratory system, and impaired MCC is a feature of many airway diseases, including both genetic (cystic fibrosis, primary ciliary dyskinesia) and acquired (chronic obstructive pulmonary disease, bronchiectasis) disorders. Research into the fundamental processes controlling MCC, therefore, has direct clinical application, but has been limited in part due to the difficulty of studying this complex multicomponent system in vitro. In this study, we have characterized a novel method that allows human airway epithelial cells to differentiate into a mucociliary epithelium that transports mucus in a continuous circular track. The mucociliary transport device allows the measurement and manipulation of all features of mucociliary transport in a controlled in vitro system. In this initial study, the effect of ciliary beat frequency and mucus concentration on the speed of mucociliary transport was investigated.


1999 ◽  
Vol 277 (3) ◽  
pp. L465-L471 ◽  
Author(s):  
Alessandro Celi ◽  
Silvana Cianchetti ◽  
Stefano Petruzzelli ◽  
Stefano Carnevali ◽  
Filomena Baliva ◽  
...  

Intercellular adhesion molecule-1 (ICAM-1) is the only inducible adhesion receptor for neutrophils identified in bronchial epithelial cells. We stimulated human airway epithelial cells with various agonists to evaluate whether ICAM-1-independent adhesion mechanisms could be elicited. Phorbol 12-myristate 13-acetate (PMA) stimulation of cells of the alveolar cell line A549 caused a rapid, significant increase in neutrophil adhesion from 11 ± 3 to 49 ± 7% (SE). A significant increase from 17 ± 4 to 39 ± 6% was also observed for neutrophil adhesion to PMA-stimulated human bronchial epithelial cells in primary culture. Although ICAM-1 expression was upregulated by PMA at late time points, it was not affected at 10 min when neutrophil adhesion was already clearly enhanced. Antibodies to ICAM-1 had no effect on neutrophil adhesion. In contrast, antibodies to the leukocyte integrin β-chain CD18 totally inhibited the adhesion of neutrophils to PMA-stimulated epithelial cells. These results demonstrate that PMA stimulation of human airway epithelial cells causes an increase in neutrophil adhesion that is not dependent on ICAM-1 upregulation.


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