The role of natural resistance in protection of the murine host from listeriosis.

Host resistance to infection with Listeria monocytogenes in the murine host can be viewed as comprising an early, non-immunologically specific phase of natural resistance, and this is followed 2-3 days later by a phase of acquired or immunologically specific cellular resistance. Recent evidence has shown that the key mechanisms underlying natural resistance are under genetic regulation: mice classed as relatively resistant demonstrate an early net bacterial growth rate which is significantly lower than that seen in strains classed as susceptible. The genetic advantage of the resistant host is attributed to the participation of a population of young (radiosensitive) immigrant mononuclear phagocytes which are protective against Listeria during the early phase of natural resistance. Mononuclear phagocyte kinetics differ markedly between resistant and susceptible strains of mice at this time. Thus, in the bone marrow, the incidence of progenitor cells for macrophage colony formation increases and the cell cycle time of promonocytes shortens in resistant, but not in susceptible, mice shortly following listerial infection. A peripheral blood monocytosis develops 24 h post-infection in resistant mice and these cells leave the blood at a more rapid rate, as shown by a fall in the half-time of monocytes in such hosts. Immigrant macrophages accumulate at a subcutaneous site of listerial infection in significantly greater numbers in resistant C57BL/6J mice as compared to susceptible A/J mice, during the phase of natural resistance. Thus, the genetically-determined high natural resistance to listeriosis can be correlated with the ability of the resistant host to mount a prompt macrophage inflammatory response, which is not evident in susceptible mice during this phase of the infection.(ABSTRACT TRUNCATED AT 250 WORDS)