Mice with a secondary Listeria monocytogenes
infection eliminate the bacteria much faster and more efficiently from their organs than mice with a primary
infection. During the course of a
secondary infection, serum concentrations of
interferon-gamma (IFN-gamma) and tumour
necrosis factor-alpha (TNF) are higher than during a primary
infection. The aim of the present study was to determine whether these
cytokines are involved in the acquired resistance to L. monocytogenes during a
secondary infection in mice. In order to neutralize
cytokines,
alginate-encapsulated cells, which form anti-
cytokine monoclonal antibodies, were injected into the nuchal region of mice during a
Listeria infection. Mice recovered from a sublethal primary
Listeria infection, which acquired cell-mediated immunity, received a
subcutaneous injection of anti-IFN-gamma-forming cells, or anti-TNF-forming cells, and 4 days later received an
intravenous injection with 10 50% lethal dose (LD50) L. monocytogenes. The number of bacteria recovered from the liver and spleen of immune mice treated with anti-IFN-gamma-forming cells was slightly larger (approximately 1 log10) than that found for immune mice treated with anti-
beta-galactosidase-forming cells, called immune control mice. The organs of immune mice treated with anti-TNF-forming cells yielded significantly more (approximately 4 log10) bacteria than those of immune control mice, more than those of immune mice treated with anti-IFN-gamma-forming cells, and comparable numbers to those of non-immune mice. Taken together, these results demonstrate that TNF is essential in acquired resistance to L. monocytogenes during a
secondary infection in mice, while IFN-gamma plays a minor role.