Infection by the intracellular parasite Listeria monocytogenes was studied in two inbred lines of mice genetically selected for high and low antibody production against xenogeneic red blood cells. It was revealed that, during the early non-specific phase of infection, bacterial growth in tissues was significantly enhanced in high responder (HR) mice, as opposed to low responder (LR) mice. This is interpreted as the in vivo expression of a genetic impairment of the bactericidal activity of resident macrophages in this line of mice. After Day 2 of infection, the kinetics of bacterial growth in the spleen and the liver was almost identical in the two lines, indicating that mice from both lines generated efficient anti-Listeria immunity. This was confirmed by the fact that no interline difference could be detected in the expression of T-cell mediated immunity, as estimated by the production of protective T cells and delayed sensitivity T cells, and by the level of immunological memory. The genetic impairment in the bactericidal activity of resident macrophages resulted in a significant increase of anti-Listeria antibody production in HR mice and did not prevent T-dependent activation of effector macrophages mobilized in infectious sites. This explains that the overall resistance to listeriosis was similar in LR and HR mice, as shown by the LD50 values respectively estimated as 2.2 X 10(5) and 3.8 X 10(5) bacteria per mouse. This natural resistance was expressed at the same level as that of C57BL/6 mice.