Abstract
Background: Cystic fibrosis is the most common life-shortening genetic disease in the Caucasian population, affecting |[sim]|1 in 2,500 births. Inheritance is AR and results from mutations in the CFTR, which functions in transepithelial salt and water regulation. In humans, lung damage is the primary source of morbidity, although exocrine pancreatic dysfunction is generally present. Difficulties in gene delivery to the mature airway epithelium and early onset airway damage provide a rationale for exploring gene therapy during lung development. In this study, we evaluated lentivirus-mediated gene transfer to cultured fetal sheep airway epithelium and lung tissue explants. Model choice was based on fetal size, a pattern of airway development that parallels the human lung, the relatively late appearance of immuno-competence and tolerance of the ovine uterus to fetal manipulation.
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