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Keicho, N., Y. Higashimoto, G. P. Bondy, W. M. Elliott, J. C. Hogg, and S. Hayashi. Endotoxin-specific NF-[Kappa]B activation in pulmonary epithelial cells harboring adenovirus E1A. Am. J. Physiol. 277 (Lung Cell. Mol. Physiol. 21): L523-L532, 1999.--Adenovirus E1A DNA and proteins are detected in lung epithelial cells of patients with chronic obstructive pulmonary disease. In investigating E1A regulation of inflammatory mediator expression in human lung epithelial cells, we found increased intercellular adhesion molecule-1 (ICAM-1) and interleukin-8 expression after lipopolysaccharide (LPS) stimulation of A549 cells stably transfected with adenovirus 5 E1A. We now show that E1A-dependent induction of interleukin-8 expression is specific to LPS, superinduced by cycloheximide, and not observed after tumor necrosis factor or phorbol 12-myristate 13-acetate stimulation. Electrophoretic mobility shift assays revealed that tumor necrosis factor or phorbol 12-myristate 13-acetate induced nuclear factor-[Kappa]B binding complexes of Rel A and p50 in E1A and control transfectants, whereas LPS was effective only in E1A transfectants. Similarly, LPS-induced nuclear translocation of nuclear factor-[Kappa]B was observed only in E1A transfectants. CCAAT-enhancer binding protein binding was undetected and activator protein-1 binding was unaffected by LPS in either cell type, whereas basal mRNA levels of c-jun were unchanged by E1A. We conclude that E1A enhances the expression of these inflammatory mediator genes by modulating events specific to LPS-triggered nuclear factor-[Kappa]B induction in these cells. A549 cells; lipopolysaccharide response; regulation of infiammatory mediator expression; nuclear factor-[Kappa]B

Presents information on a study which detected a type of adenovirus DNA and proteins in lung epithelial cells of patients with chronic obstructive pulmonary disease. Methodology and materials; Results; Conclusion.