Reduced interleukin-18 secretion in Brucella abortus 2308-infected murine peritoneal macrophages and in spleen cells obtained from B. abortus 2308-infected mice.

Th1 immune responses in which gamma interferon (IFN-gamma) production predominates are associated with protective immunity against intracellular bacteria. Following infection, interleukin-18 (IL-18) may contribute, in association with IL-12, to optimal IFN-gamma production. In this study, the secretion of IL-18 following intracellular infection with virulent Brucella abortus 2308 in CD-1 cultured peritoneal macrophages and splenocyte cultures was investigated. The production of IL-18 was reduced in both CD-1 mouse peritoneal macrophages infected with B. abortus 2308 and splenocyte cultures obtained from B. abortus 2308-infected mice at 3, 6 and 10 days post-infection (p.i.). In contrast, splenocyte cultures obtained from B. abortus 2308-infected mice at 3 days p.i. secreted significant amounts of IFN-gamma. Stimulation of these cells with recombinant IL-18 (rIL-18) and/or rIL-12 did not significantly increase IFN-gamma secretion at the splenocyte level. These data suggest that once the infection has been established, B. abortus 2308 selectively limits IL-18 secretion without affecting endogenous IFN-gamma production.