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B and MAP
kinase pathways in human colonic myofibroblasts
Department of Internal Medicine, Shiga University of Medical Science, Otsu 520-2192, Japan
Colonic
subepithelial myofibroblasts (SEMFs) may play a role in the modulation
of mucosal inflammatory responses. We investigated the effects of
interleukin (IL)-17 on IL-6 and chemokine [IL-8 and monocyte
chemoattractant protein (MCP)-1] secretion in colonic SEMFs. Cytokine
expression was determined by ELISA and Northern blotting. Nuclear
factor kappa B (NF-
B) DNA-binding activity was evaluated by
electrophortetic gel mobility shift assay (EMSA). The activation of
mitogen-activated protein kinase (MAPK) was assessed by immunoblotting.
IL-6, IL-8, and MCP-1 secretions were rapidly induced by IL-17. IL-17
induced NF-B activation within 45 min after stimulation. A blockade
of NF-B activation markedly reduced these responses. MAPK inhibitors
(SB-203580, PD-98059, and U-0126) significantly reduced the
IL-17-induced IL-6 and chemokine secretion. The combination of either
IL-17 + IL-1
or IL-17 + tumor necrosis factor (TNF)-
enhanced cytokine secretion; in particular, the effects of IL-17 + TNF- on IL-6 secretion were much stronger than the other responses.
This was dependent on the enhancement of IL-6 mRNA stability. In
conclusion, human SEMFs secreted IL-6, IL-8, and MCP-1 in response to
IL-17. These responses might play an important role in the pathogenesis
of gut inflammation.
inflammation; chemokine; inflammatory bowel disease
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