1887

Abstract

Th1 immune responses in which gamma interferon (IFN-γ) 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-γ production. In this study, the secretion of IL-18 following intracellular infection with virulent 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 2308 and splenocyte cultures obtained from 2308-infected mice at 3, 6 and 10 days post-infection (p.i.). In contrast, splenocyte cultures obtained from 2308-infected mice at 3 days p.i. secreted significant amounts of IFN-γ. Stimulation of these cells with recombinant IL-18 (rIL-18) and/or rIL-12 did not significantly increase IFN-γ secretion at the splenocyte level. These data suggest that once the infection has been established, 2308 selectively limits IL-18 secretion without affecting endogenous IFN-γ production.

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2005-06-01
2020-10-22
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