scholarly journals Role of ENaC and of the Na/K pump on the Hypertonicity‐induced inhibition of Na Transport in Cystic Fibrosis Human Bronchial Epithelial Cells

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Hector Rasgado-Flores ◽  
Thierry Ngansop ◽  
Paul Piennette ◽  
Kevin Gallegos ◽  
Robert J Bridges
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Na Transport ◽  
Bronchial Epithelial

scholarly journals Differentiation of human bronchial epithelial cells: role of hydrocortisone in development of ion transport pathways involved in mucociliary clearance

2016 ◽  
Vol 311 (2) ◽  
pp. C225-C236 ◽  
Author(s):  
Nathan A. Zaidman ◽  
Angela Panoskaltsis-Mortari ◽  
Scott M. O'Grady
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Mucociliary Clearance ◽  
Bronchial Epithelium ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Transport Pathways ◽  
Bronchial Epithelial ◽  
Normal Human

Glucocorticoids strongly influence the mucosal-defense functions performed by the bronchial epithelium, and inhaled corticosteroids are critical in the treatment of patients with inflammatory airway diseases such as asthma, chronic obstructive pulmonary disease, and cystic fibrosis. A common pathology associated with these diseases is reduced mucociliary clearance, a defense mechanism involving the coordinated transport of salt, water, and mucus by the bronchial epithelium, ultimately leading to retention of pathogens and particles in the airways and to further disease progression. In the present study we investigated the role of hydrocortisone (HC) in differentiation and development of the ion transport phenotype of normal human bronchial epithelial cells under air-liquid interface conditions. Normal human bronchial epithelial cells differentiated in the absence of HC (HC0) showed significantly less benzamil-sensitive short-circuit current than controls, as well as a reduced response after stimulation with the selective β2-adrenergic receptor agonist salbutamol. Apical membrane localization of epithelial Na+ channel α-subunits was similarly reduced in HC0 cells compared with controls, supporting a role of HC in the trafficking and density of Na+ channels in the plasma membrane. Additionally, glucocorticoid exposure during differentiation regulated the transcription of cystic fibrosis transmembrane conductance regulator and β2-adrenergic receptor mRNAs and appeared to be necessary for the expression of cystic fibrosis transmembrane conductance regulator-dependent anion secretion in response to β2-agonists. HC had no significant effect on surface cell differentiation but did modulate the expression of mucin mRNAs. These findings indicate that glucocorticoids support mucosal defense by regulating critical transport pathways essential for effective mucociliary clearance.

scholarly journals Role of S1P/S1PR3 axis in release of CCL20 from human bronchial epithelial cells

PLoS ONE ◽  
2018 ◽  
Vol 13 (9) ◽  
pp. e0203211 ◽  
Author(s):  
Yoshitaka Kawa ◽  
Tatsuya Nagano ◽  
Asuka Yoshizaki ◽  
Ryota Dokuni ◽  
Masahiro Katsurada ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

Role of PARP-1 on B(a)P induced DNA methylation variation in human bronchial epithelial cells

2010 ◽  
Vol 196 ◽  
pp. S177-S178
Author(s):  
Z.X. Zhuang ◽  
G.H. Tao ◽  
C.M. Gong ◽  
L.Q. Yang ◽  
H.Y. Huang ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Parp 1 ◽  
Methylation Variation

Role of CREB in vasoactive intestinal peptide-mediated wound healing in human bronchial epithelial cells

2009 ◽  
Vol 153 (1-3) ◽  
pp. 64-69 ◽  
Author(s):  
Cha-Xiang Guan ◽  
Yan-Ru Cui ◽  
Guo-Ying Sun ◽  
Fang Yu ◽  
Chun-Yan Tang ◽  
...  
Keyword(s):  
Wound Healing ◽  
Epithelial Cells ◽  
Vasoactive Intestinal Peptide ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

Inhibition of chloride secretion in human bronchial epithelial cells by cigarette smoke extract

2005 ◽  
Vol 288 (5) ◽  
pp. L894-L902 ◽  
Author(s):  
James L. Kreindler ◽  
Alan D. Jackson ◽  
Philip A. Kemp ◽  
Robert J. Bridges ◽  
Henry Danahay
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Ion Transport ◽  
Cigarette Smoke ◽  
Apical Membrane ◽  
Chloride Secretion ◽  
Cigarette Smoke Extract ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

Chronic bronchitis, a disease mainly of cigarette smokers, shares many clinical features with cystic fibrosis, a disease of altered ion transport, suggesting that the negative effects of cigarette smoke on mucociliary clearance may be mediated through alterations in ion transport. We tested the hypothesis that cigarette smoke extract would inhibit chloride secretion in human bronchial epithelial cells. In agreement with studies in canine trachea, cigarette smoke extract inhibited net chloride secretion without affecting sodium transport. We performed microelectrode impalements and impedance analysis studies to investigate the physiological mechanisms of this inhibition. These data demonstrated that cigarette smoke extract caused an acute increase in membrane resistances in conjunction with apical membrane hyperpolarization, an effect consistent with inhibition of an apical membrane anion conductance. After this acute phase, both membrane resistances decreased while membrane potentials continued to hyperpolarize, indicating that cigarette smoke extract also inhibited the basolateral entry of chloride into the cell. Furthermore, cigarette smoke extract caused an increase in mucin secretion. Therefore, the ion transport phenotype of human bronchial epithelial cells exposed to cigarette smoke extract is similar to that of cystic fibrosis epithelia in which there is sodium absorption out of proportion to chloride secretion in the setting of increased mucus secretion.

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