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B-Inducing Kinase Is a Common Mediator of IL-17-, TNF-
-, and IL-1ß-Induced Chemokine Promoter Activation in Intestinal Epithelial Cells1
Gastrointestinal Unit, Department of Medicine, Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114
IL-17 expression is restricted to activated T cells, whereas the
IL-17R is expressed in a variety of cell types including intestinal
epithelial cells. However, the functional responses of intestinal
epithelial cells to stimulation with IL-17 are unknown. Moreover, the
signal transduction pathways activated by the IL-17R have not been
characterized. IL-17 induced NF-
B protein-DNA complexes consisting
of p65/p50 heterodimers in the rat intestinal epithelial cell line
IEC-6. The induction of NF-B correlated with the induction of CXC
and CC chemokine mRNA expression in IEC-6 cells. IL-17 acted in a
synergistic fashion with IL-1ß to induce the NF-B site-dependent
CINC promoter. Induction of the CINC promoter by IL-17 in IEC-6 cells
was TNF receptor-associated factor-6 (TRAF6), but not TRAF2, dependent.
Furthermore, IL-17 induction of the CINC promoter could be inhibited by
kinase-negative mutants of NF-B-inducing kinase and IB
kinase-
. In addition to activation of the NF-B, IL-17 regulated
the activities of extracellular regulated kinase, c-Jun N-terminal
kinase, and p38 mitogen-activated protein kinases in IEC-6 cells.
Whereas the IL-17-mediated activation of extracellular regulated kinase
mitogen-activated protein kinases was mediated through
ras, c-Jun N-terminal kinase activation was dependent on
functional TRAF6. These data suggest that NF-B-inducing kinase
serves as the common mediator in the NF-B signaling cascades
triggered by IL-17, TNF-, and IL-1ß in intestinal epithelial
cells.
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