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B in the Transcriptional Control of Cyclooxygenase-2 Expression by IFN-
in Macrophages1
Centro de Biología Molecular "Severo Ochoa," Consejo Superior de Investigaciones Científicas-Universidad Autónoma, Madrid, Spain
IFN-
induces cyclooxygenase (COX)-2 expression and PG production in mouse macrophage cells. IFN- activates COX-2 promoter-driven transcription. Deletion of the IFN sequence regulatory element (ISRE) I –1541/–1522 and ISRE II –1215/–1206 sites of the mouse COX-2 promoter minimally decrease this IFN- induction. In contrast, deletion of the –965/–150 region from the COX-2 promoter abrogated IFN- induction. In this region a NF-
B site has been described and mutation of this site impairs the induction of the full COX-2 promoter by IFN-. Moreover, IFN- induction of the COX-2 promoter was also strongly reduced by transfection of plasmid encoding the NF-B inhibitor, IB
. Interestingly, IFN- induction of the COX-2 and PGE2 synthesis was absent in macrophages from TNF–/– mice, and neutralizing anti-TNF Abs inhibited COX-2 promoter induction by IFN- in RAW 264.7 macrophages. Moreover, NF-B activity was induced late after stimulation with IFN- correlating with the effect of autocrine TNF, and this NF-B activation was absent in macrophages from TNF–/– mice. Taken together our results suggest a model in which IFN--induced TNF activates NF-B, which is required for full COX-2 expression.
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