The adenovirus e1a 13s gene product up regulates the tnf gene. Metcalf, Jordan P. Pulmonary and Critical Care Division, Department of Internal Medicine, University of Oklahoma Health Sciences Center, and the Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma
APStracts 2:0206L, 1995.
TNF is a potential mediator of adenovirus-mediated lung inflammation. I postulated that early genes of adenovirus transactivate the TNF gene as a possible mechanism. To examine this hypothesis, I transfected T-lymphocyte-like Jurkat cells and monocyte/macrophage -like THP-1 cells with plasmids coding for adenovirus E1A 12S or 13S proteins along with a plasmid containing the TNF promoter linked to chloramphenicol acetyltransferase (CAT). In unstimulated Jurkat cells E1A 13S increased TNF CAT activity 21 fold over cells transfected with control E1A plasmid while 12S had a minimal effect. In unstimulated THP-1 cells 13S increased TNF CAT activity by almost 2 fold over cells transfected with the control E1A plasmid; 12S had no effect. The effect of 13S was present in both cell lines when stimulated (Jurkat cells; PMA, THP-1 cells; LPS). E1A 13S also increased endogenous TNF mRNA production in LPS stimulated THP-1 cells. These studies show adenovirus E1A 13S stimulates the TNF gene in inflammatory cell lines. 

Received 6 April 1995; accepted in final form 19 October 1995.
APS Manuscript Number L106-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95