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J Med Microbiol 54 (2005), 527-531; DOI: 10.1099/jmm.0.45936-0
© 2005 Society for General Microbiology
ISSN 0022-2615

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

Luis Fernández-Lago1, Antonio Orduña2 and Nieves Vizcaíno1

1Departamento de Microbiología y Genética, Edificio Departamental, Universidad de Salamanca, Plaza Doctores de la Reina s/n, 37007 Salamanca, Spain 2Departamento de Microbiología, Facultad de Medicina, Universidad de Valladolid, Valladolid, Spain

Correspondence Luis Fernández-Lago lrlago{at}usal.es

Received October 21, 2004
Accepted February 4, 2005

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.

Abbreviations: HK, heat-killed; i.p., intraperitoneal; p.i., post-infection; S-LPS, smooth lipopolysaccharide.






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