scholarly journals Human bronchial epithelial cells exposed in vitro to cigarette smoke at the air-liquid interface resemble bronchial epithelium from human smokers

2013 ◽  
Vol 304 (7) ◽  
pp. L489-L503 ◽  
Author(s):  
Carole Mathis ◽  
Carine Poussin ◽  
Dirk Weisensee ◽  
Stephan Gebel ◽  
Arnd Hengstermann ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Bronchial Epithelium ◽  
Bronchial Epithelial Cells ◽  
Liquid Interface ◽  
Gene Set Enrichment Analysis ◽  
Bronchial Epithelial ◽  
In Vitro System ◽  
Air Liquid Interface

Organotypic culture of human primary bronchial epithelial cells is a useful in vitro system to study normal biological processes and lung disease mechanisms, to develop new therapies, and to assess the biological perturbations induced by environmental pollutants. Herein, we investigate whether the perturbations induced by cigarette smoke (CS) and observed in the epithelium of smokers' airways are reproducible in this in vitro system (AIR-100 tissue), which has been shown to recapitulate most of the characteristics of the human bronchial epithelium. Human AIR-100 tissues were exposed to mainstream CS for 7, 14, 21, or 28 min at the air-liquid interface, and we investigated various biological endpoints [e.g., gene expression and microRNA profiles, matrix metalloproteinase 1 (MMP-1) release] at multiple postexposure time points (0.5, 2, 4, 24, 48 h). By performing a Gene Set Enrichment Analysis, we observed a significant enrichment of human smokers' bronchial epithelium gene signatures derived from different public transcriptomics datasets in CS-exposed AIR-100 tissue. Comparison of in vitro microRNA profiles with microRNA data from healthy smokers highlighted various highly translatable microRNAs associated with inflammation or with cell cycle processes that are known to be perturbed by CS in lung tissue. We also found a dose-dependent increase of MMP-1 release by AIR-100 tissue 48 h after CS exposure in agreement with the known effect of CS on this collagenase expression in smokers' tissues. In conclusion, a similar biological perturbation than the one observed in vivo in smokers' airway epithelium could be induced after a single CS exposure of a human organotypic bronchial epithelium-like tissue culture.

Structural and functional variations in human bronchial epithelial cells cultured in air-liquid interface using different growth media

2020 ◽  
Vol 318 (5) ◽  
pp. L1063-L1073 ◽  
Author(s):  
Clarus Leung ◽  
Samuel J. Wadsworth ◽  
S. Jasemine Yang ◽  
Delbert R. Dorscheid
Keyword(s):  
Epithelial Cells ◽  
Respiratory Disease ◽  
Cell Cultures ◽  
Bronchial Epithelium ◽  
Barrier Properties ◽  
Bronchial Epithelial Cells ◽  
Liquid Interface ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Air Liquid Interface

The human bronchial epithelium is an important barrier tissue that is damaged or pathologically altered in various acute and chronic respiratory conditions. To represent the epithelial component of respiratory disease, it is essential to use a physiologically relevant model of this tissue. The human bronchial epithelium is a highly organized tissue consisting of a number of specialized cell types. Primary human bronchial epithelial cells (HBEC) can be differentiated into a mucociliated tissue in air-liquid interface (ALI) cultures using appropriately supplemented media under optimized growth conditions. We compared the histology, ciliary length, and function, diffusion, and barrier properties of HBEC from donors with no respiratory disease grown in two different media, PneumaCult-ALI or Bronchial Epithelial Differentiation Medium (BEDM). In the former group, HBEC have a more physiological pseudostratified morphology and mucociliary differentiation, including increased epithelial thickness, intracellular expression of airway-specific mucin protein MUC5AC, and total expression of cilia basal-body protein compared with cells from the same donor grown in the other medium. Baseline expression levels of inflammatory mediators, thymic stromal lymphopoietin (TSLP), soluble ST2, and eotaxin-3 were lower in PneumaCult-ALI. Additionally, the physiological cilia beat frequency and electrical barrier properties with transepithelial electrical resistance were significantly different between the two groups. Our study has shown that these primary cell cultures from the same donor grown in the two media possess variable structural and functional characteristics. Therefore, it is important to objectively validate primary epithelial cell cultures before experimentation to ensure they are appropriate to answer a specific scientific question.

scholarly journals Expression of lipocortins in human bronchial epithelial cells: effects of IL-1β , TNF-α, LPS and dexamethasone

1996 ◽  
Vol 5 (3) ◽  
pp. 210-217
Author(s):  
M. M. Verheggen ◽  
H. I. M. de Bont ◽  
P. W. C. Adriaansen-Soeting ◽  
B. J. A. Goense ◽  
C. J. A. M. Tak ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bronchial Epithelium ◽  
Northern Blotting ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Annexin I ◽  
Tnf Α

In this study, we investigated the expression of lipocortin I and II (annexin I and I in the human bronchial epithelium, bothin vivoandin vitro. A clear expression of lipocortin I and II protein was found in the epithelium in sections of bronchial tissue. In cultured human bronchial epithelial cells we demonstrated the expression of lipocortin I and II mRNA and protein using Northern blotting, FACScan analysis and ELISA. No induction of lipocortin I or II mRNA or protein was observed after incubation with dexamethasone. Stimulation of bronchial epithelial cells with IL-1β, TNF-α or LPS for 24 h did not affect the lipocortin I or II mRNA or protein expression, although PGE2and 6-keto-PGF1αproduction was significantly increased. This IL-1β- and LPS-mediated increase in eicosanoids could be reduced by dexamethasone, but was not accompanied by an increase in lipocortin I or II expression. In human bronchial epithelial cells this particular glucocorticoid action is not mediated through lipocortin I or II induction.

scholarly journals Bronchial epithelium in children: a key player in asthma

2016 ◽  
Vol 25 (140) ◽  
pp. 158-169 ◽  
Author(s):  
Ania Carsin ◽  
Julie Mazenq ◽  
Alexandra Ilstad ◽  
Jean-Christophe Dubus ◽  
Pascal Chanez ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Inflammation ◽  
Ex Vivo ◽  
Bronchial Epithelium ◽  
Bronchial Epithelial Cells ◽  
Physical Barrier ◽  
Bronchial Epithelial ◽  
Immunological Properties ◽  
Physical Chemical

Bronchial epithelium is a key element of the respiratory airways. It constitutes the interface between the environment and the host. It is a physical barrier with many chemical and immunological properties. The bronchial epithelium is abnormal in asthma, even in children. It represents a key component promoting airway inflammation and remodelling that can lead to chronic symptoms. In this review, we present an overview of bronchial epithelium and how to study it, with a specific focus on children. We report physical, chemical and immunological properties fromex vivoandin vitrostudies. The responses to various deleterious agents, such as viruses or allergens, may lead to persistent abnormalities orchestrated by bronchial epithelial cells. As epithelium dysfunctions occur early in asthma, reprogramming the epithelium may represent an ambitious goal to induce asthma remission in children.

Sign in / Sign up

Export Citation Format

Share Document