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Department of Internal Medicine, Shiga University of Medical Science, Seta Tukinowa, Otsu, Japan
There is increasing evidence that IL-6 plays an important role in
the pathophysiology of acute pancreatitis via its broad proinflammatory
actions. To identify the local biosynthetic site for IL-6 in human
pancreas, we investigated IL-6 secretion in human pancreatic periacinar
myofibroblasts. IL-6 secretion was determined by ELISA and Northern
blotting. The activation of NF-
B was assessed by EMSA. The
activation of mitogen-activated protein kinase (MAPK) was assessed by
immunoblotting. IL-6 secretion was rapidly induced by IL-17, IL-1
,
and TNF-
. EMSAs demonstrated that IL-17, IL-1, and TNF-
induced NF-B activation within 1.5 h after stimulation, and a
blockade of NF-B activation by the pyrrolidine derivative of
dithiocarbamate and tosyl-phe-chloromethylketone markedly reduced the
IL-17-, IL-1-, or TNF--induced IL-6 gene expression. Furthermore,
IL-17, IL-1, and TNF- induced a rapid activation of extracellular
signal-related kinase p42/44 and p38 MAPKs, and specific MAPK
inhibitors (SB203580, PD98059, and U0216) significantly reduced IL-17-,
IL-1-, or TNF--induced IL-6 secretion, indicating the role of
MAPKs in the induction of IL-6. The combination of either IL-17 plus
IL-1 or IL-17 plus TNF- enhanced IL-6 secretion and IL-6 mRNA
expression; in particular, the effects of IL-17 plus TNF- were much
stronger than those induced by IL-17 plus IL-1. TNF--induced IL-6
mRNA degraded rapidly at any concentrations, and the combination of
IL-17 and TNF- markedly enhanced IL-6 mRNA stability. This indicates
that the effects of IL-17 plus TNF- were regulated at the
post-transcriptional level. In conclusion, pancreatic periacinar
myofibroblasts secreted a large amount of IL-6 in response to
proinflammatory cytokines. These cells might play an important role in
the pathogenesis of acute pancreatitis via IL-6
secretion.
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