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/ß Attenuates the Expression of Inducible Nitric Oxide Synthase Through a Decrease in NF-
B Activation1
*
Instituto de Bioquímica (Centro Mixto Consejo Superior de Investigaciones Cientificas-Universidad Compluteuse de Madrid), Facultad de Farmacia, Universidad Complutense, Madrid, Spain; and
Centro de Química Farmacéutica, Habana, Cuba
Triggering peritoneal macrophages with IFN-
and a low
concentration of LPS induced the expression of the inducible form of
nitric oxide synthase (iNOS). This process was significantly inhibited
when IFN-
/ß was added during the initial 2 h after the start
of IFN-/LPS activation. Evaluation of the transcriptional activity
using run-on assays indicated that IFN-/ß inhibited the
transcription of iNOS. Transfection experiments using a 1.7-kb promoter
sequence corresponding to the 5' flanking region of the murine iNOS
gene showed decreased promoter activity in the presence of type I IFNs.
Analysis of the transcription factors that participate in iNOS
expression revealed a marked decrease of NF-
B activation, a nuclear
factor required for the transcription of this gene. The degradation of
IB and IBß, which is required for the translocation of
NF-B to the nucleus, was inhibited in the presence of IFN-/ß.
However, the activity of other transcription factors such as IFN
regulatory factor 1, which is involved in the expression of iNOS in
response to IFN-, was not affected by IFN-/ß stimulation. These
results suggest that in the presence of IFN-/ß, the activity of
the iNOS promoter is impaired, and this attenuated nitric oxide
synthase expression could be important in pathophysiologic situations
in which secretion of type I IFNs occurs.
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