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-Inducing Factor) Regulates Early Cytokine Production in, and Promotes Resolution of, Bacterial Infection in Mice1
*
Max von Pettenkofer Institut, Ludwig-Maximilians-Universität, Munich, Germany;
Hayashibara Biochemical Laboratories, Inc., Fujisaki Institute, Okayama, Japan; and
Department of Bacteriology, Hyogo College of Medicine, Nishinomiyya, Japan
IL-12-induced IFN-
production is essential for clearance of
Yersinia enterocolitica infection. Similar to IL-12, the
recently described cytokine IL-18 (IFN--inducing factor) is produced
by macrophages and induces IFN- production in spleen cells.
Therefore, we have investigated the role of IL-18 in
Yersinia infection of mice. Heat-killed yersinia-triggered
IL-18-promoted IFN- production of splenocytes was predominantly
dependent on endogenous IL-12 production, whereas IL-12-promoted
IFN- production was not IL-18 dependent. IL-18-induced IFN-
production was to a higher degree dependent on IFN-R-mediated
mechanisms and in synergism with IL-2 resulted in at least fivefold
higher IFN- levels as compared with the combination of IL-12 plus
IL-2. Analysis of the effect of IL-18 on IL-12 production of
LPS-stimulated peritoneal macrophages revealed that IL-18 decreased
LPS-induced IL-12 production, indicating that IL-18 might be involved
in negative regulation of IL-12 production. In vivo studies revealed
that Yersinia-resistant C57BL/6 mice expressed fourfold
higher IL-18 mRNA levels than did susceptible BALB/c mice.
Administration of anti-IL-18 Abs caused a 100- to 1000-fold
increase in bacterial counts in the spleen of infected mice but did not
change IFN- production levels. Taken together, our data demonstrate
that IL-18 is involved in regulation of cytokine production during the
early phase of bacterial infections as well as in clearance of
Yersinia infection.
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