Genetic control of murine listeriosis expressed in the macrophage response

Susceptibility to murine listeriosis is genetically regulated. For example, A/J, C3H, CBA, DBA/1, DBA/2 and 129/J mouse strains are classed as susceptible and demonstrate an early net bacterial growth rate which is significantly higher than that seen in strains classed as resistant, namely, C57BL-derived strains, NZB and SJL. These strain differences in susceptibility are expressed during the phase of natural resistance, as a property of the macrophage response. Genetic analysis in progeny derived from resistant C57BL-derived strains and susceptible A/J or BALB/c strain mice has indicated that a major gene is responsible for determining resistance/susceptibility to listeria. The genetic advantage of the resistant phenotype is attributed to a prompt influx of young (radiosensitive) inflammatory macrophages which control the early bacterial multiplication in infective sites. Such cells reportedly have superior listericidal activity in vitro, as compared to mature macrophages. Mononuclear phagocyte production, emigration and accumulation at infective foci are all increased in resistant C57BL, but not in susceptible A/J mice, shortly following infection. Thus, resistance to listeriosis is associated with an efficient macrophage inflammatory response and, conversely, susceptibility is attributed to a sluggish response. Genetic studies have demonstrated linkage between these two traits (listeria resistance/susceptibility and the macrophage inflammatory response). In all probability, different gene loci are responsible for susceptibility amongst the various mouse strains. In A/J mice, susceptibility is attributed to C5 deficiency (specified by Hc locus) while, for C5-sufficient strains, another genetic defect is presumably responsible.(ABSTRACT TRUNCATED AT 250 WORDS)