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* Faculty of Medicine, First Department of Internal Medicine, University of the Ryukyus, Okinawa, Japan;
First Department of Internal Medicine, Kurume University, Kurume, Japan;
R&D Laboratories, Nippon Organon K. K., and
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan
The present study was conducted to critically determine the
protective role of IL-18 in host response to Mycobacterium
tuberculosis infection. IL-18-deficient (knockout (KO)) mice
were slightly more prone to this infection than wild-type (WT) mice.
Sensitivity of IL-12p40KO mice was lower than that of IL-12p40/IL-18
double KO mice. IFN-
production caused by the infection was
significantly attenuated in IL-18KO mice compared with WT mice, as
indicated by reduction in the levels of this cytokine in sera, spleen,
lung, and liver, and its synthesis by spleen cells restimulated with
purified protein derivatives. Serum IL-12p40 level postinfection and
its production by peritoneal exudate cells stimulated with live bacilli
were also significantly lower in IL-18KO mice than WT mice, suggesting
that attenuated production of IFN- was secondary to reduction of
IL-12 synthesis. However, this was not likely the case, because
administration of excess IL-12 did not restore the reduced IFN-
production in IL-18KO mice. In further studies, IL-18 transgenic mice
were more resistant to the infection than control littermate mice, and
serum IFN- level and its production by restimulated spleen cells
were increased in the former mice. Taken together, our results indicate
that IL-18 plays an important role in Th1 response and host defense
against M. tuberculosis infection although the
contribution was not as profound as that of
IL-12p40.
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