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1 Department of Internal Medicine, University of Iowa, Iowa City, IA, USA
2 Department of Microbiology, Universtiy of Iowa, Iowa City, IA, USA
3 Department of Internal Medicine, University of Colorado, Denver, CO, USA
4 Howard Hughes Medical Institute, Iowa City, IA, USA; Department of Internal Medicine, University of Iowa, Iowa City, IA, USA
* To whom correspondence should be addressed. E-mail: joseph-zabner{at}uiowa.edu.
In this study, we utilized the reverse transcriptase component of telomerase, hTERT, and human papillomavirus type 16 (HPV-16) E6 and E7 genes to transform both normal and cystic fibrosis human airway epithelial cells (HAE). One cell line, designated NuLi-1 (Normal Lung, university of iowa), was derived from HAE of normal genotype, whereas three cell lines, designated CuFi (Cystic Fibrosis, university of iowa) -1, -3, and 4, were derived from HAE of various cystic fibrosis genotypes. When grown at air liquid interface, the cell lines were capable of forming polarized differentiated epithelia that exhibited transepithelial resistance and maintained the ion channel physiology expected for the genotypes. The CFTR defect in the CuFi lines could be corrected by infecting from the basolateral surface using adenoviral vectors. We also demonstrated, by using NF
B promoter reporter constructs, that the NuLi and CuFi cell lines retained NFB responses to LPS. These cell lines should therefore be useful as models for studying ion physiology, therapeutic intervention for cystic fibrosis, and innate immunity.
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