Lung and Airway Cells: First-Line Barriers to the Outside World
Breathing air is something we do without thinking. But while we go about our day, our respiratory systems are hard at work extracting oxygen from the air and protecting the internal environment from pathogens and irritants. The first barrier to the air and its contents is the airway epithelium, a layer of epithelial cells that lines the trachea, bronchi, and lung alveoli. These cells are the first to encounter respiratory viruses, other pathogens, and pollutants, and enact host defenses to combat these challenges. Importantly, disruption of airway epithelial homeostasis can lead to conditions like asthma, which results from inflammation of the airway and causes narrowing of the airway.
Our catalog includes the following lung and airway cells, complete with optimized media for each cell type:
- Small airway epithelial cells (BronchiaLife™ media)
- Diseased bronchial/tracheal epithelial cells (BronchiaLife™ media)
- Diseased small airway epithelial cells (BronchiaLife™ media)
- Lung microvascular endothelial cells (VascuLife® media)
- Bronchial/tracheal epithelial cells (BronchiaLife™ media)
- Lung fibroblasts (FibroLife® media)
- Bronchial/tracheal smooth muscle cells (VascuLife® media)
- Lobar bronchial epithelial cells (BronchiaLife™ media)
- Lung smooth muscle cells (VascuLife® media)
Lifeline® Lung and Airway Cells in Asthma Research
Senescence is often called biological aging and occurs when a cell loses its ability to grow and proliferate. Senescence can occur over time, but can also be induced by inflammatory stimuli or oxidative stress. In particular, cell senescence of airway epithelial cells contributes to the pathogenesis of asthma. Integrin b4 (ITGB4), a cell surface protein, is decreased in the airway epithelial cells of patients with asthma. To determine whether airway epithelial cell senescence in asthma is due to loss of ITGB4, Yuan and colleagues characterized the role of ITGB4 in airway epithelial cells using in vitro and in vivo models.
First, the group used Lifeline® normal human bronchial epithelial (HBE) cells to evaluate the expression of ITGB4 in response to the inflammatory cytokine TNFa or in response to oxidative stress following O3 treatment. Their results showed that ITGB4 expression decreased following treatment with either TNFa or O3, and both treatments induced cell senescence.
To determine whether the loss of ITGB4 in vivo results in senescence, the authors next examined the airway of mice lacking ITGB4 only in airway epithelial cells. They found that compared with control mice, airway epithelial cells in mice lacking ITGB4 (airway-only knockout) were more senescent and less proliferative. Using HBE cells with siRNA-mediated loss of ITGB4, the researchers found that loss of ITGB4 in vitro resulted in increased senescence, cell cycle inhibition, and decreased anti-oxidative activity.
The p53 signaling pathway is a classic stimulator of senescence. To determine whether p53 induced senescence in HBE cells in the absence of ITGB4, the authors evaluated cellular senescence following ITGB4 and p53 knockdown. As expected, they found that loss of p53 reduced ITGB4 knockdown-induced senescence.
Together, the results of this study suggest that reduced expression of ITGB4 following inflammation or oxidative stress results in p53-mediated cell senescence.
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