Induction of the epidermal growth factor receptor and its ligands in nasal epithelium by ozone.

Background: Ozone is a photochemical oxidant pollutant that is an important public health hazard. Although the inflammatory response that occurs in response to ozone inhalation is well characterized, the mechanisms underlying epithelial cell activation are not well understood.

Objective: Because the epidermal growth factor receptor (EGFR) is a central regulator of epithelial function, we tested the hypothesis that nasal epithelial cells respond to ozone-induced oxidant stress by modulating expression of the EGFR and its ligands, EGF and transforming growth factor-alpha (TGF-alpha).

Matrix metalloproteinases and their inhibitors in the nasal mucosa of patients with perennial allergic rhinitis.

Background: Allergic rhinitis and asthma show many similarities in their epithelial and inflammatory responses to allergens. However, one notable difference is that disruption and desquamation of the epithelium is a characteristic feature of asthma, whereas in perennial allergic rhinitis the epithelium is intact and thickened. One reason for this might be differing expression of matrix metalloproteinases (MMPs) or their inhibitors (TIMPs).

Interaction of cigarette smoke and house dust mite allergens on inflammatory mediator release from primary cultures of human bronchial epithelial cells.

Several studies have shown that exposure to cigarette smoke and/or house dust mite (HDM) can lead to increased airway inflammation in susceptible individuals. The underlying mechanisms, however, are not defined. To investigate the interaction between cigarette smoke and HDM allergen on mediator release from primary cultures of human bronchial epithelial cells.

Cigarette smoke decreases the expression of secretory component in human bronchial epithelial cells, in vitro.

Epithelial secretory component (SC) is thought to be essential for immunologic protection of the respiratory tract from viral and bacterial infection, since it transports polymeric IgA from the basolateral to the luminal surface of epithelial cells. We have hypothesized that recurrent infection in airways of cigarette smokers is at least partly a consequence of cigarette smoke-induced downregulation of the expression and/or release of SC from airway epithelial cells, subsequently resulting in decreased transcytosis of secretory IgA to the airway lumen. To test this hypothesis, we have cultured human bronchial epithelial cells (HBEC) from surgical tissues and exposed these for 20 minutes to either air or cigarette smoke.

Effect of Variable Inspiratory Flow Rate on the Performance of the Budesonide Rhinocort Turbuhaler™.

Objective: To investigate the effect of variable nasal inspiratory flow rates in vitro on total drug delivery and deposition patterns of budesonide delivered from the Rhinocort Turbuhaler™.

Methods: The total dose of budesonide delivered at flow rates of 15, 30 and 60 L/min and the particle size distribution of the delivered drug at flow rates of 28 and 60 L/min were determined at regular intervals throughout the life of six Rhinocort Turbuhalers™, each containing 200 × 100μ,g doses of budesonide. The delivered dose was determined by drawing individual doses of budesonide through separate G0120 Filtrete electrostatic filters.