title: Endogenous interleukin-12 is involved in resistance to Brucella abortus infection.
abstract: 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.
authors.affiliation: Department of Microbiology, University of Melbourne, Parkville, Victoria, Australia.
authors.forename: Y
authors.initials: Y
authors.lastname: Zhan
authors.forename: C
authors.initials: C
authors.lastname: Cheers
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D002003:Brucella abortus / Q000276:immunology*; D002006:Brucellosis / Q000276:immunology*; D005260:Female; D007111:Immunity, Cellular; D007158:Immunologic Techniques; D007371:Interferon-gamma / Q000096:biosynthesis*; D018664:Interleukin-12 / Q000502:physiology*; D008264:Macrophages / Q000276:immunology*; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA; D009569:Nitric Oxide / Q000378:metabolism; D013154:Spleen / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D018664:Interleukin-12; D009569:Nitric Oxide; D007371:Interferon-gamma