The difference in natural resistance to
Salmonella typhimurium between
S. typhimurium-resistant A/J mice and
S. typhimurium-susceptible C57BL/6 mice was analyzed. In both strains, the growth of
S. typhimurium was controlled in the spleen until 48hr of infection, while serum C3b levels were increased in A/J mice immediately after infection but not in C57BL/6mice. Incubation of A/J mouse serum with
S. typhimurium or its lipopolysaccharide (LPS) generated sufficient amounts of C3b, but that of C57BL/6 mouse serum with them did not. A/J macrophages had higher intracellular killing activity
in vitro than did C57BL/6 cells against
S. typhimurium pre-opsonized with each corresponding fresh serum. However, the cells from both mice exhibited a similar level of killing activity against
S. typhimurium pre-opsonized with fresh A/J serum or rabbit complement. The resistance of C57BL/6 mice was significantly increased by opsonizing
S. typhimurium with fresh A/J serum or rabbit complement before inoculation. The serum level of interferon-γ (IFN-γ) in A/J mice was 2.7 times as high as in C57BL/6 mice at 48hr post-infection. Recombinant murine IFN-γ enhanced the intracellular killing activity of macrophages from both mice when
S. typhimurium was pre-opsonized with fresh A/J serum but not with fresh C57BL/6 serum. These findings suggest that A/J macrophages exhibit maximal killing activity against A/J serum-opsonized
S. typhimurium in vivo when the cells are activated with IFN-γ. Therefore, the rapid and sufficient activation of complement by
Salmonella LPS may render A/J mice more resistant against murine typhoid.
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