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*
Department of Microbiology and Immunology, School of Dentistry, and
Department of Animal Production Science, Graduate School of Agricultural Science, Tohoku University, Sendai, Japan;
Laboratory of Host Defenses, Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Japan;
Seiryo Dental Clinic, Sendai, Japan; and
¶ T-Cell Research Institute, Sendai, Japan
IL-18, a potent IFN-
-inducing cytokine, is expressed by various
nonimmune cells as well as macrophages, suggesting that it has
important physiological and immunological roles. The present study
focused on the mechanism of active IL-18 induction from human oral
epithelial cells. The epithelial cells and the cell lines
constitutively express IL-18 mRNA and the 24-kDa precursor form of
IL-18. Bioactive IL-18 exhibiting IFN--inducing activity was
detected in the supernatant of the cells on costimulation with
neutrophil proteinase 3 (PR3) and LPS for 24 h after
IFN--priming for 3 days. An active 18-kDa form of IL-18 was detected
in lysate and supernatant of the cells only after the above treatment
and the induction was inhibited by cycloheximide and by serine
proteinase inhibitors. After the treatment, lactate dehydrogenase
activity was not detected in the cell culture supernatant, and PR3 was
detected only in the membrane and not in cytoplasm fractions of the
cells. Caspase-1 was not detected in the cells even after the treatment
and the IL-18 induction was not inhibited by a caspase-1 inhibitor.
These results suggest that the PR3-mediated induction of bioactive
IL-18 secretion from oral epithelial cells in combination with LPS
after IFN--priming occurred via a caspase-1-independent pathway, and
provide new insight into the possible involvement of a neutrophil
proteinase in the induction of bioactive IL-18 in oral inflammation
such as periodontitis.
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