scholarly journals Molecular insights into the physiology of the ‘thin film’ of airway surface liquid

1999 ◽  
Vol 516 (3) ◽  
pp. 631-638 ◽  
Author(s):  
R. C. Boucher
Keyword(s):  
Thin Film ◽  
Airway Surface Liquid ◽  
Surface Liquid

A Comparison of the Elemental Concentrations Obtained using X-ray Microanalysis of Bulk Cryofractured and Ultrathin Cryosectioned Mucus Layer of the Airway Surface Liquid in Mouse Trachea

2001 ◽  
Vol 7 (S2) ◽  
pp. 998-999
Author(s):  
C.A. Ackerley ◽  
G. Kent ◽  
Y.M. Heng ◽  
A. Tilups ◽  
L.E. Becker
Keyword(s):  
Thin Film ◽  
Filter Paper ◽  
Airway Surface Liquid ◽  
Mucus Layer ◽  
X Ray ◽  
Major Function ◽  
Cellular Debris ◽  
Surface Liquid ◽  
The Individual ◽  
Pathological Material

The airways are lined with a thin film consisting of two layers. A watery layer, the airway surface liquid (ASL) surrounds the cilia and its major function is to serve as a medium for ciliary boating of mucus out of the respiratory system. The other layer is a viscous mucus layer consisting mainly of airway cellular secretions and cellular debris.The composition and effects of altered concentrations of the constitutive elements in the ASL and mucus layer remain a mystery. in human patients, attempts have been made to determine the composition of these layers by sampling with a filter paper by touching it to the mucosa and wetting it by capillary action. This material was then removed from the filter paper and quantitative analyses using energy dispersive x-ray spectrometry (EDS) and a Hall’s thin film correction routine performed on the residue. Although differences were detected between normal and pathological material, these results did not reflect the composition of the individual layers but an average of both.Attempts have been made to determine the elemental composition of these layers in intact and in cultured rabbit trachea, bovine trachea and hamster trachea.

Development of Confocal Reflection Microscopy for the Study of Airway Surface Liquid Dysregulation in Cystic Fibrosis

Pneumologie ◽  
2015 ◽  
Vol 69 (07) ◽  
Author(s):  
A Seyhan Agircan ◽  
M Lampe ◽  
J Duerr ◽  
R Pepperkok ◽  
MA Mall
Keyword(s):  
Cystic Fibrosis ◽  
Airway Surface Liquid ◽  
Surface Liquid

Hyperinflammation and airway surface liquid dehydration in cystic fibrosis: purinergic system as therapeutic target

2021 ◽  
Author(s):  
Thiago Inácio Teixeira do Carmo ◽  
Victor Emanuel Miranda Soares ◽  
Jonatha Wruck ◽  
Fernanda dos Anjos ◽  
Débora Tavares de Resende e Silva ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Therapeutic Target ◽  
Airway Surface Liquid ◽  
Purinergic System ◽  
Surface Liquid

Airway Absorption of Soluble Gases. A Method of Measuring Airway Surface Liquid?

1985 ◽  
Vol 69 (s12) ◽  
pp. 33P-33P
Author(s):  
P.S. Woolman ◽  
T.W. Higenbottam ◽  
D. Shaw
Keyword(s):  
Airway Surface Liquid ◽  
Surface Liquid

IL-13 acidifies airway surface liquid pH via an omeprazole inhibitable mechanism

2018 ◽  
Vol 141 (2) ◽  
pp. AB123
Author(s):  
Jin Young Min ◽  
Julia He Huang ◽  
James E. Norton ◽  
Lydia A. Suh ◽  
Caroline P.E. Price ◽  
...  
Keyword(s):  
Airway Surface Liquid ◽  
Surface Liquid

Airway surface liquid thickness as a function of lung volume in small airways of the guinea pig

1994 ◽  
Vol 77 (5) ◽  
pp. 2333-2340 ◽  
Author(s):  
D. Yager ◽  
T. Cloutier ◽  
H. Feldman ◽  
J. Bastacky ◽  
J. M. Drazen ◽  
...  
Keyword(s):  
Surface Tension ◽  
Epithelial Cells ◽  
Guinea Pig ◽  
Cross Sections ◽  
Lung Volume ◽  
Longitudinal Direction ◽  
Small Airways ◽  
Airway Surface Liquid ◽  
Residual Capacity ◽  
Surface Liquid

The average thickness and distribution of airway surface liquid (ASL) on the luminal surface of peripheral airways were measured in normal guinea pig lungs frozen at functional residual capacity (FRC) and total lung capacity (TLC). Tissue blocks containing cross sections of airways of internal perimeter 0.188–3.342 mm were cut from frozen lungs and imaged by low-temperature scanning electron microscopy (LTSEM). Measurements made from LTSEM images were found to be independent of freezing rate by comparison of measurements at rapid and slow freezing rates. At both lung volumes, the ASL was not uniformly distributed in either the circumferential or longitudinal direction; there were regions of ASL where its thickness was < 0.1 micron, whereas in other regions ASL collected in pools. Discernible liquid on the surfaces of airways frozen at FRC followed the contours of epithelial cells and collected in pockets formed by neighboring cells, a geometry consistent with a low value of surface tension at the air-liquid interface. At TLC airway liquid collected to cover epithelial cells and to form a liquid meniscus, a geometry consistent with a higher value of surface tension. The average ASL thickness (h) was approximately proportional to the square root of airway internal perimeter, regardless of lung volume. For airways of internal perimeter 250 and 1,800 microns, h was 0.9 and 1.8 microns at FRC and 1.7 and 3.7 microns at TLC, respectively. For a given airway internal perimeter, h was 1.99 times thicker at TLC than at FRC; the difference was statistically significant (P < 0.01; 95% confidence interval 1.29–3.08).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals SPLUNC1 degradation by the cystic fibrosis mucosal environment drives airway surface liquid dehydration

2018 ◽  
Vol 52 (4) ◽  
pp. 1800668 ◽  
Author(s):  
Megan J. Webster ◽  
Boris Reidel ◽  
Chong D. Tan ◽  
Arunava Ghosh ◽  
Neil E. Alexis ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Airway Surface Liquid ◽  
The Novel ◽  
Pulmonary Tissue ◽  
Tissue Samples ◽  
Protein Levels ◽  
Surface Liquid ◽  
Protease Degradation ◽  
Mucosal Secretions ◽  
Cystic Fibrosis Transmembrane

The multi-organ disease cystic fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane regulator gene (CFTR) that lead to diminished transepithelial anion transport. CF lungs are characterised by airway surface liquid (ASL) dehydration, chronic infection/inflammation and neutrophilia. Dysfunctional CFTR may upregulate the epithelial Na+ channel (ENaC), further exacerbating dehydration. We previously demonstrated that short palate lung and nasal epithelial clone 1 (SPLUNC1) negatively regulates ENaC in normal airway epithelia.Here, we used pulmonary tissue samples, sputum and human bronchial epithelial cells (HBECs) to determine whether SPLUNC1 could regulate ENaC in a CF-like environment.We found reduced endogenous SPLUNC1 in CF secretions, and rapid degradation of recombinant SPLUNC1 (rSPLUNC1) by CF secretions. Normal sputum, containing SPLUNC1 and SPLUNC1-derived peptides, inhibited ENaC in both normal and CF HBECs. Conversely, CF sputum activated ENaC, and rSPLUNC1 could not reverse this phenomenon. Additionally, we observed upregulation of ENaC protein levels in human CF bronchi. Unlike SPLUNC1, the novel SPLUNC1-derived peptide SPX-101 resisted protease degradation, bound apically to HBECs, inhibited ENaC and prevented ASL dehydration following extended pre-incubation with CF sputum.Our data indicate that CF mucosal secretions drive ASL hyperabsorption and that protease-resistant peptides, e.g. SPX-101, can reverse this effect to rehydrate CF ASL.

Sign in / Sign up

Export Citation Format

Share Document