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Production in Response to Live or Dead Bacteria by TNF and Other Factors1
Department of Microbiology, University of Melbourne, Parkville, Victoria, Australia
When mice were infected i.v. with either Listeria
monocytogenes or Brucella abortus, bioactive
IL-12 was briefly detected in serum and supernatants of spleen
homogenates immediately ex vivo. Although the time scale was more
prolonged for the more slowly growing B. abortus, in
both instances IL-12 production ceased while bacteria still persisted
in high numbers. Production of IL-12, detected in serum and spleen, was
neither increased nor prolonged by injecting Abs to IL-10 or IL-4. In
contrast with live organisms, heat-killed bacteria did not induce
detectable IL-12 in vivo and were less efficient when added in vitro to
resident peritoneal cells or spleen cells. Mice lacking the receptors
for TNF (TNFR-/- mice) were severely deficient in IL-12 production,
suggesting a controlling role for TNF, which we have previously shown
to be triggered by live, rather than dead, bacteria. Infection in the
TNFR-/- mice was exacerbated, although in the
Brucella-infected mice splenomegaly, the main indicator
of immunopathology, was reduced. Production of NO by macrophages was
deficient, but the TNFR-/- mice were not deficient in IFN-
production. In addition to being poor inducers of IL-12, killed
bacteria actively suppressed IL-12 production in response to live
bacteria, by mechanism(s) unknown. The implications of these findings
are discussed in light of the fact that only live bacteria
satisfactorily induce cell-mediated immunity to
infection.
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