Abstract
In mice pre-treated with Corynebacterium parvum, Listeria monocytogenes was cleared rapidly from the blood and bacterial growth in the liver and spleen was inhibited effectively during the early phase of infection. This enhanced resistance could be transferred with peritoneal exudate cells (PEC) but not with non-adherent spleen cells. In spite of earlier elimination of bacteria, pre-treated mice developed lower levels of delayed-type hypersensitivity (DTH) to bacteria than untreated immune control mice, but the control levels of DTH could be reached by increasing the challenge dose of bacteria in C. parvum-pre-treated mice. Additionally, C. parvum did not inhibit the expression of antibacterial immunity when immune mice were rechallenged. It appeared that the active suppression of the T-cell mediated immune response by C. parvum-activated macrophages was not seen during the course of L. monocytogenes infection, and that the lower levels of DTH seen in mice pre-treated with C. parvum were attributable to an insufficient antigenic stimulus following the accelerated elimination of bacteria by non-specifically activated macrophages during the early phase of infection.
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