Development of cystic fibrosis and noncystic fibrosis airway cell lines

被引:139
|
作者
Zabner, J [1 ]
Karp, P
Seiler, M
Phillips, SL
Mitchell, CJ
Saavedra, M
Welsh, M
Klingelhutz, AJ
机构
[1] Univ Iowa, Dept Internal Med, Iowa City, IA 52242 USA
[2] Univ Iowa, Dept Microbiol, Iowa City, IA 52242 USA
[3] Univ Iowa, Howard Hughes Med Inst, Iowa City, IA 52242 USA
[4] Univ Colorado, Dept Internal Med, Denver, CO 80262 USA
关键词
cystic fibrosis transmembrane conductance regulator; human papillomavirus type 16; human airway epithelial cells; telomerase;
D O I
10.1152/ajplung.00355.2002
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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-kappaB promoter reporter constructs, we also demonstrated that the NuLi and CuFi cell lines retained nuclear factor-kappaB responses to lipopolysaccharide. These cell lines should therefore be useful as models for studying ion physiology, therapeutic intervention for CF, and innate immunity.
引用
收藏
页码:L844 / L854
页数:11
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