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B activation in pulmonary epithelial
cells harboring adenovirus E1A
1 Pulmonary Research Laboratory, University of British Columbia, Vancouver, British Columbia, Canada V6Z 1Y6; and 2 Third Department of Internal Medicine, University of Tokyo, Tokyo 113, Japan
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-
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-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-B induction in these cells.
A549 cells; lipopolysaccharide response; regulation of inflammatory
mediator expression; nuclear factor-B
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