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Institutes of
*
Immunology and
Pathology, College of Veterinary Medicine, University of Leipzig, Leipzig, Germany
To study a potential IL-12p40-dependent but IL-12p75-independent
agonistic activity regulating the immune response against
Salmonella Enteritidis, the course of infection in
IL-12p35-deficient mice (IL-12p35-/-, capable of
producing IL-12p40) was compared with that of IL-12p40-/-
mice. Mice lacking IL-12p40 revealed a higher mortality rate and higher
bacterial organ burden than mice capable of producing IL-12p40. This
phenotype was found in both genetically susceptible (BALB/c,
Itys) and resistant mice (129Sv/Ev,
Ityr) indicating
Ity-independent mechanisms. The more effective control
of bacteria in the IL-12p35-/- mice was associated with
elevated serum IFN-
and TNF-
levels. In contrast,
IL-12p40-/- mice showed reduced IFN- production, which
was associated with significantly elevated serum IgE levels. Early
during infection (days 3 and 4 postinfection), as well as late (day 20
postinfection), the number of infected phagocytes was strongly
increased in the absence of IL-12p40 indicating impaired bactericidal
activity when IL-12p40 was missing. Liver histopathology revealed a
decreased number of mononuclear granulomas in IL-12p40-/-
mice. Depletion of CD4+ or CD8+ T
lymphocytes in vivo suggested that both T cell subpopulations
contribute to the IL-12p40-dependent protective functions. Analysis of
IL-12p40 vs IL-23p19 mRNA expression revealed an up-regulation of only
IL-12p40 mRNA during Salmonella infection. Together
these data indicate that IL-12p40 can induce protective mechanisms
during both the innate and the adaptive type 1 immune response in
Salmonella infection. This novel activity of IL-12p40
complements the well described dominant and essential role of IL-12p75
in protective immunity to Salmonella
infection.
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