Previous Article | Next Article ![]()
Journal of Virology, May 1999, p. 4502-4507, Vol. 73, No. 5
Division of Pulmonary Medicine, Children's
Hospital Research Foundation, Cincinnati, Ohio 45229-3039
Received 20 October 1998/Accepted 19 January 1999
Respiratory syncytial virus (RSV) infection of airway epithelial
cells results in persistent NF-
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Incomplete Regulation of NF-
B by I
B
during
Respiratory Syncytial Virus Infection in A549 Cells
B activation and NF-
B-mediated interleukin-8 production. Previous studies in airway epithelial cells
demonstrated that tumor necrosis factor alpha (TNF-
)-induced NF-
B
activation is transient due to regulation by I
B
. However, during
RSV infection, I
B
has only a partial inhibitory effect on NF-
B
activation. Studies presented here demonstrate that neither increased
I
B
production which occurs as a result of RSV-induced NF-
B
activation nor inhibition of proteasome-mediated I
B
degradation results in a reversal of RSV-induced NF-
B activation. Thus, while manipulation of I
B
results in reversal of TNF-
-induced NF-
B activation, manipulation of I
B
does not result in a reversal of
RSV-induced NF-
B activation.
*
Corresponding author. Mailing address: Division of
Pulmonary Medicine, Children's Hospital Research Foundation, 3333 Burnet Ave., Cincinnati, OH 45229-3039. Phone: (513) 636-6771. Fax:
(513) 636-4615. E-mail: FIEDM0{at}CHMCC.ORG.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»