Cellular mechanisms in the protection against infection by Listeria monocytogenes in mice.

Listeria monocytogenes, in doses of 2-0 X 10(3) to 3-0 X 10(3) viable organisms, was injected into athymic nude mice, irradiated mice and mice treated with reticuloendothelial system-blocking agents. Viable counts on liver and spleen homogenates were made at intervals after infection. In both nude mice (nu/nu) and normal littermates (nu/+) of BALB/c background, the bacteria grew rapidly for 24 h but increased only slowly thereafter, to reach a plateau of about 10(5) per organ at 72 h. In nu/+ mice, the number of viable bacteria began to decrease after 6 to 9 days, with complete elimination by day 12. In nude mice, the number of Listeria remained at a stable level of approximately 10(5) per organ during the observation period of 21 days. In lethally irradiated nu/+ mice, bacteria grew progressively and extensively to reach 10(7) per spleen and 10(9) per liver by 72 h. Bacterial growth during the first 72 h was markedly enhanced by treatment with carbon particles, dextran sulphate 500 or silica. These enhancing effects were also observed in nude mice and in AKR, C3H/He and C57BL/6 animals. We conclude that both non-immune phagocytes and T cell-dependent mechanisms contribute to the resistance of mice to Listeria infection.