Superantigens stimulate
T-cell-receptor Vbeta-selective T-cell proliferation accompanying the release of
cytokines, which may eventually protect the host from microbial
infections. We investigated here whether
superantigens can rescue the host from lethal
bacterial infection. Mice were pretreated with Staphylococcus aureus
enterotoxin B (SEB) 1 and 2 days before
bacterial infection, and the mortality of infected mice was assessed. SEB pretreatment protected mice from lethal
infection with Listeria monocytogenes but not from lethal
infection with Streptococcus pyogenes. This enhanced protection was also observed upon pretreatment with recombinant
streptococcal pyrogenic exotoxin A. Furthermore, L. monocytogenes-specific delayed-type
hypersensitivity (DTH) due to type 1 helper T (Th1) cells and the cytotoxicity of CD8(+) T cells were significantly enhanced after SEB administration and
bacterial infection. Depletion of either CD4(+) T cells or CD8(+) T cells in SEB-pretreated mice completely abolished this protection. This phenomenon was ascribed to the elimination of L. monocytogenes-specific CD8(+) cytotoxic T lymphocytes (CTL). It was found that CD4(+) T cells contributed to the induction of the CTL populations. Furthermore, SEB pretreatment of heat-killed L. monocytogenes-immunized mice enhanced the protection from challenge of L. monocytogenes. Taken together, these results indicated that administrations of
superantigens protected mice from
infection with L. monocytogenes, which was dependent on the enhanced L. monocytogenes-specific CTL activity in the presence of CD4(+) T cells, and
superantigens exhibited adjuvant activity in the immunization against intracellular pathogens.