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Departments of 1 Internal Medicine and 2 Microbiology, 3 Howard Hughes Medical Institute, University of Iowa, Iowa City, Iowa 52242; and 4 Department of Internal Medicine, University of Colorado, Denver, Colorado 80262
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 normal and
cystic fibrosis (CF) human airway epithelial (HAE) cells. One cell
line, designated NuLi-1 (normal lung, University of Iowa), was derived
from HAE of normal genotype; three cell lines, designated CuFi (cystic
fibrosis, University of Iowa)-1, CuFi-3, and CuFi-4, were derived from
HAE of various CF genotypes. When grown at the 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 CF transmembrane
conductance regulator defect in the CuFi cell lines could be corrected
by infecting from the basolateral surface using adenoviral vectors.
Using nuclear factor-
B promoter reporter constructs, we also
demonstrated that the NuLi and CuFi cell lines retained nuclear
factor-B responses to lipopolysaccharide. These cell lines should
therefore be useful as models for studying ion physiology, therapeutic
intervention for CF, and innate immunity.
cystic fibrosis transmembrane conductance regulator; human papillomavirus type 16; human airway epithelial cells; telomerase
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