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*
Laboratory of Cellular and Molecular Immunology, Department of Animal Health and Biomedical Sciences, and
Enzyme Institute, Research Animal Resource Center, University of Wisconsin, Madison, WI 53706
IFN-
is a key cytokine controlling Brucella
infection, and the diverse functions of this cytokine are mediated by
IFN regulatory factors (IRFs) such as IRF-1, IRF-2, and IFN consensus
sequence binding protein (ICSBP). However, the roles of these three
IRFs in Brucella infection have not been investigated.
The infection of each IRF-deficient mouse strain provides an
opportunity to determine not only the significance of each IRF molecule
but also the crucial immune components necessary for host defense
during in vivo infection, because respective IRF-deficient mouse
strains contain unique immunodeficient phenotypes.
Brucella abortus S2308-infected
IRF-1-/- mice were dead within 2 wk postinfection, while
IRF-2-/- mice contained less splenic
Brucella CFU than wild-type mice at the early stage of
infection. Infected ICSBP-/- mice maintained a plateau of
splenic Brucella CFU throughout the infection.
Additional infection of IL-12p40-, NO synthase 2-, and
gp91phox-deficient mice indicates that these
immune components are crucial for Brucella immunity and
may contribute to the susceptibility of IRF-1-/- and
ICSBP-/- mice. Immunologic and histopathological analyses
of infected IRF-1-/- mice indicate that the absence of
IL-12p40 induction and serious hepatic damage are involved in the death
of IRF-1-/- mice. These results indicate that 1) IRF-1
and ICSBP are essential transcriptional factors for IFN--mediated
protection against Brucella; 2) IL-12, reactive nitrogen
intermediates, and reactive oxygen intermediates are crucial immune
components against Brucella, and their absence may
contribute to the susceptibility of IRF-1-/- and
ICSBP-/- mice; and 3) hepatic damage caused by
Brucella virulence contributes to the death of
IRF-1-/- mice.
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