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Gene Expression by TNF-Dependent NF-
B Activation1
* Department of Obstetrics and Gynecology, Nagasaki University School of Medicine, and Nagasaki University Medical Skill Junior College, Nagasaki, Japan; and
Division of Cytokine Signaling, Department of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Medical Sciences, Nagasaki, Japan
Macrophage-inflammatory protein-3
(MIP-3), also designated as
liver and activation-regulated chemokine (LARC), Exodus, or CCL20, is a
recently identified CC chemokine that is expected to play a crucial
role in the initiation of immune responses. In this study, we describe
that MIP-3 expression is under the direct control of NF-
B, a key
transcription factor of immune and inflammatory responses.
Overexpression of the p65/RelA subunit of NF-B significantly
increased the MIP-3 mRNA level. MIP-3 transcription was
stimulated by TNF, and this stimulation was inhibited by an NF-B
inhibitor, I-B superrepressor. Analysis of the human MIP-3
promoter demonstrated a functional NF-B site responsible for its
expression. We also show that MIP-3 expression is induced in
LPS-treated mouse livers that were primed with Propionibacterium
acnes, which developed massive liver injury with infiltration
of inflammatory cells. This induction was fully dependent on the TNF
signaling cascade, because it was not observed in the livers of
TNFR1-deficient mice. Furthermore, pretreatment with gliotoxin, an
inhibitor of NF-B activity, abrogated the P.
acnes/LPS-induced MIP-3 expression of wild-type mice. These
results clearly demonstrate that MIP-3 gene expression is dependent
on NF-B activity in vitro, and indicate that the TNFR1-mediated TNF
signaling cascade that leads to NF-B activation plays an essential
role in MIP-3 expression in the murine liver injury
model.
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