The natural resistance of radiation chimeras to S. typhimurium C5

Differences in the in vivo net growth rate of Salmonella typhimurium C5 during the first week of infection in different mouse strains are controlled by a single autosomal gene. In lethally irradiated mice repopulated with semi-allogeneic bone marrow, the early net growth rate shows the phenotype of the donor of the bone marrow cell and not the phenotype of the irradiated recipient. Thus, genetically controlled differences in in vivo bacterial net growth rate are a consequence of mechanisms operating in cells which have originated from bone marrow precursors. Natural resistance to S. typhimurium C5 requires, in addition to slow net growth rate, other mechanisms which come into operation at the end of the first week of the infection. These later acting processes are more complex and can not be transferred to susceptible mice using bone marrow cells alone.