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1
,§,**
*
First Department of Surgery,
Department of Immunology & Medical Zoology,
Department of Otolaryngology,
§
Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Japan;
¶
Department of Immunology, National Institute of Animal Health, Tsukuba, Japan;
||
Institute for Microbial Diseases, Osaka University, Suita, Japan;
#
Vertex Pharmaceuticals, Cambridge, MA 02139; and
**
Core Research for Evolutional Science and Technology of Japan Science and Technology Corporation, Tokyo, Japan
IL-18, produced as biologically inactive precursor, is secreted
from LPS-stimulated macrophages after cleavage by caspase-1. In this
study, we investigated the mechanism underlying caspase-1-mediated
IL-18 secretion. Kupffer cells constantly stored IL-18 and
constitutively expressed caspase-1. Inhibition of new protein synthesis
only slightly reduced IL-18 secretion, while it decreased and abrogated
their IL-1
and IL-12 secretion, respectively. Kupffer cells
deficient in Toll-like receptor (TLR) 4, an LPS-signaling receptor, did
not secrete IL-18, IL-1, and IL-12 upon LPS stimulation. In
contrast, Kupffer cells lacking myeloid differentiation factor 88
(MyD88), an adaptor molecule for TLR-mediated-signaling, secreted IL-18
without IL-1 and IL-12 production in a caspase-1-dependent and de
novo synthesis-independent manner. These results indicate that MyD88 is
essential for IL-12 and IL-1 production from Kupffer cells while
their IL-18 secretion is mediated via activation of endogenous
caspase-1 without de novo protein synthesis in a MyD88-independent
fashion after stimulation with LPS. In addition, infection with
Listeria monocytogenes, products of which have the
capacity to activate TLR, increased serum levels of IL-18 in wild-type
and MyD88-deficient mice but not in caspase-1-deficient mice, whereas
it induced elevation of serum levels of IL-12 in both wild-type and
caspase-1-deficient mice but not in MyD88-deficient mice. Taken
together, these results suggested caspase-1-dependent,
MyD88-independent IL-18 release in bacterial
infection.
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