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Human airway barrier studies

Rothen-Rutishauser B, Blank F, Mtihlfeld C et al (2008) In vitro models of the human epithelial airway barrier to study the toxic potential of particulate matter. Expert Opin Drug Metab Toxicol 4 1075-1089... [Pg.448]

Human exposure to a combination of tobacco smoke and the house dust mites has been shown to result in allergic sensitization. It is believed that tobacco smoke impairs the barrier function of the airway epithelium, leading to increased access of allergens contained in the house dust mite. In vitro studies with human bronchial epithelial cells have confirmed this hypothesis. I42,43l In this instance it is believed that lipophiles in tobacco smoke serve to facilitate the permeation of toxic allergens. [Pg.423]

We used in vitro models of lung epithelial cell lines or primary cells to determine E25 permeability. Two different cell types were used to mimic the airway and alveolar epithelium of the lung to study transport. Calu-3, a human cell line derived from an airway carcinoma, when grown at an air/liquid interface, differentiate to form a secretory airway epithelium (17). Rat primary epithelial cells isolated as described by Cheek et al. (18) form a tight barrier similar in structure and function to the alveolar surface. Both cell types when grown to confluence form tight junctions and differentiate and polarize so that the apical or air surface has different characteristics than the basolateral or blood side. The typical transepithelial resistance observed was 350 or >1000 ohms-cm for Calu-3 cells or primary rat alveolar cells, respectively. Once an acceptable resistance was achieved, E25 (2 mg/mL) was placed in either the apical or the basolateral chamber. Cell monolayers were incubated at 37°C for up to 3 hours and ELISA measured the amount of E25 that translocated the epithelial layer and appeared in the receiver well. The apparent permeability (Papp) of the epithelium for E25 was calculated as ... [Pg.286]


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See also in sourсe #XX -- [ Pg.433 ]




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