Barrier disrupting effects of alternaria alternata extract on bronchial epithelium from asthmatic donors.

Sensitization and exposure to the allergenic fungus Alternaria alternata has been associated with increased risk of asthma and asthma exacerbations. The first cells to encounter inhaled allergens are epithelial cells at the airway mucosal surface. Epithelial barrier function has previously been reported to be defective in asthma.

TNF-α-mediated bronchial barrier disruption and regulation by src-family kinase activation.

Background: Because TNF-α is increased in severe asthma, we hypothesized that TNF-α contributes to barrier dysfunction and cell activation in bronchial epithelial cells. We further hypothesized that src-family kinase inhibition would improve barrier function in healthy cells in the presence of TNF-α and directly in cultures of severe asthmatic cells where the barrier is disrupted.

Objectives: We assessed the effect of TNF-α, with or without src-family kinase inhibitor SU6656, on barrier properties and cytokine release in differentiated human bronchial epithelial cultures.

Barrier responses of human bronchial epithelial cells to grass pollen exposure.

The airway epithelium forms a physical, chemical and immunological barrier against inhaled environmental substances. In asthma, these barrier properties are thought to be abnormal. In this study, we analysed the effect of grass pollen on the physical and immunological barrier properties of differentiated human primary bronchial epithelial cells.

Mechanisms of immunotherapy in allergic rhinitis.

Allergic rhinitis is a common condition, but many people still experience suboptimal control of symptoms despite measures such as allergen avoidance, intra-nasal steroids and antihistamines. Specific immunotherapy (SIT) has been used for many years, but though many studies show clinical efficacy, its mechanism of action is still not clearly understood. Earlier studies showed changes in antibodies and it may be that SIT works through mechanisms that alter the ratio of 'protective' IgG4 to 'pro-allergenic' IgE.