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Vol. 294, Issue 2, 548-554, August 2000
B/Rel in
Lipopolysaccharide-Stimulated Macrophages1
Korea Research Institute of Bioscience and Biotechnology, Yusong,
Taejon, Korea
We show that radicicol, a fungal antibiotic, produces a marked
inhibition of p38 kinase, nuclear factor-
B/Rel (NF-B/Rel), and
inducible nitric-oxide synthase (iNOS) transcription by the macrophage
line RAW 264.7 in response to lipopolysaccharide (LPS). Treatment of
RAW 264.7 with radicicol inhibited LPS-stimulated p38 kinase
phosphorylation in a dose-related manner. iNOS transcription, which is
regulated in part by the NF-B/Rel family of transcription factors,
has been shown to be under the control of the p38 kinase signaling
cascade. Our data also show that the p38 kinase pathway is specifically
involved in LPS-induced NF-B/Rel activation and iNOS expression
because NF-B/Rel DNA binding and iNOS mRNA production in the
presence of a specific inhibitor of p38 kinase, SB203580, were
dramatically diminished. In contrast, PD98059, a specific inhibitor of
mitogen-activated protein kinase/extracellular signal-regulated protein
kinase kinase 1 had no effect on NF-B/Rel activation and iNOS
expression. LPS-induced loss of inhibitory proteins IB-
and
IB-
and translocation of p65, c-Rel, and p50 was inhibited by radicicol. Collectively, this series of experiments indicates that
radicicol inhibits iNOS gene expression by blocking p38 kinase signaling. Due to the critical role that NO release plays in mediating inflammatory responses, the inhibitory effects of radicicol on iNOS
suggest that this potent antifungal agent may represent a useful
anti-inflammatory agent.
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