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Infect. Immun., Apr 1995, 1387-1390, Vol 63, No. 4
Y Zhan and C Cheers
Protective immunity against Brucella abortus is mediated by acquired
cellular resistance, with gamma interferon (IFN-gamma)-producing T cells
playing a key role. Interleukin-12 (IL-12) is a cytokine that has a
profound effect on the induction of IFN-gamma-producing Th1 and NK cells.
Here we report that depletion of endogenous IL-12 before infection of mice
significantly exacerbated brucella infection. IL-12- depleted mice also had
reduced splenomegaly resulting from infection and showed a decrease in
percentage and absolute numbers of macrophages compared with those in
control infected mice. Furthermore, spleen cells from IL-12-depleted mice
had a reduced ability to produce nitrite, a product of activated
macrophages. This could be the result of the low production of IFN-gamma by
splenic T cells observed in the IL-12- depleted mice. The mechanism whereby
IL-12 controls antibacterial resistance is discussed.
Copyright © 1995, American Society for Microbiology
Endogenous interleukin-12 is involved in resistance to Brucella abortus infection
Department of Microbiology, University of Melbourne, Parkville, Victoria, Australia.
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