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

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.

3D Printing of Neural Tissues Derived from Human Induced Pluripotent Stem Cells Using a Fibrin-Based Bioink.

3D bioprinting offers the opportunity to automate the process of tissue engineering, which combines biomaterial scaffolds and cells to generate substitutes for diseased or damaged tissues. These bioprinting methods construct tissue replacements by positioning cells encapsulated in bioinks into specific locations in the resulting constructs. Human induced pluripotent stem cells (hiPSCs) serve as an important tool when engineering neural tissues.

Gene expression analysis in asthma using a targeted multiplex array.

Background: Gene expression changes in the structural cells of the airways are thought to play a role in the development of asthma and airway hyperresponsiveness. This includes changes to smooth muscle contractile machinery and epithelial barrier integrity genes. We used a targeted gene expression arrays to identify changes in the expression and co-expression of genes important in asthma pathology.

Fluticasone Induces Epithelial Injury and Alters Barrier Function in Normal Subjects.

Objective: The airway epithelium has a number of roles pivotal to the pathogenesis of asthma, including provision of a physical and immune barrier to the inhaled environment. Dysregulated injury and repair responses in asthma result in loss of airway epithelial integrity. Inhaled corticosteroids are a corner stone of asthma treatment.

A new transcriptional role for matrix metalloproteinase-12 in antiviral immunity.

Interferon-α (IFN-α) is essential for antiviral immunity, but in the absence of matrix metalloproteinase-12 (MMP-12) or IκBα (encoded by NFKBIA) we show that IFN-α is retained in the cytosol of virus-infected cells and is not secreted. Our findings suggest that activated IκBα mediates the export of IFN-α from virus-infected cells and that the inability of cells in Mmp12(-/-) but not wild-type mice to express IκBα and thus export IFN-α makes coxsackievirus type B3 infection lethal and renders respiratory syncytial virus more pathogenic. We show here that after macrophage secretion, MMP-12 is transported into virus-infected cells.

Personalised medicine and asthma diagnostics/management.

Human beings come in all shapes and sizes. Heterogeneity makes life interesting, but leads to inter-individual variation in disease susceptibility and response to therapy. One major health challenge is to develop "personalised medicine"; therapeutic interventions tailored to an individual to ensure optimal treatment of disease.

The airway epithelium in asthma: developmental issues that scar the airways for life?

While allergies are very common, affecting ∼40% of the population in most Western countries, only a proportion of allergic people develop asthma. This highlights the importance of tissue and cell specific mechanisms that contribute to the disease. As the interface between the inhaled environment and the internal environment of the lung, the epithelium normally possesses numerous mechanisms to maintain an effective protective barrier.

IL-13 and TH2 cytokine exposure triggers matrix metalloproteinase 7-mediated Fas ligand cleavage from bronchial epithelial cells.

Background: Bronchial epithelial damage and activation likely contribute to the inflammatory and airway-remodeling events characteristic of severe asthma. Interaction of Fas receptor (CD95) with its ligand (FasL; CD95L) is an important mechanism of cell-mediated apoptosis. Bronchial epithelial FasL expression provides immune barrier protection from immune cell-mediated damage.

Glucocorticoids increase repair potential in a novel in vitro human airway epithelial wounding model.

Airway epithelial damage is a cardinal feature of chronic asthma. Agents which enhance epithelial repair without triggering uncontrolled fibrosis of the mesenchyme would be predicted to be useful in the management of asthma. We have developed a repeat wound model using mucociliated human bronchial epithelial cell (HBEC) cultures to define the key pathways involved in airway epithelial repair, and to study the effects of potential therapeutic agents on epithelial repair in a chronic setting.