Constitutive Activation of PrfA Tilts the Balance of Listeria monocytogenes Fitness Towards Life within the Host versus Environmental Survival
Figure 5
Growth of the prfA* mutants in the livers and spleens of intravenously infected mice.
7–8 week old ND4 Swiss Webster mice were infected with L. monocytogenes via tail-vein injections, and at the specified times post-infection (pi), the bacterial loads of the livers and spleens were determined as described in Experimental Procedures. Data are presented as scatter dot plots, with horizontal bars representing means. (A) Infection of mice with 2×104 CFU wild type, prfA G155S, prfA L140F, or prfA G145S mutants. Organs were harvested 24 hours pi. Asterisks denote statistically significant differences between the amounts of prfA* mutant and wild type CFU recovered using a one-way analysis of variance with Dunnett's post-test (*, P<0.05; ***, P<0.001). (B) Comparison of infection with 2×103 or 2×104 CFU of wild type and prfA G145S mutant. Organs were harvested 48 hours pi. Asterisks denote statistically significant differences between the amounts of prfA G145S mutant and wild type CFU recovered using an unpaired t test with a two-tailed P value (**, P<0.01). (C) Competitive index of wild type and prfA* strains. Prior to intravenous injection, the wild type Ermr reference strain and the indicated test strain were mixed 1∶1 for a total bacterial suspension of 2×104 CFU. For each organ, the competitive index (CI) value (CI = test strain CFU/reference strain CFU) was determined as described in Experimental Procedures. Asterisks denote statistically significant CI values compared to 1 using a one-sample t test with a two-tailed P value (*, P<0.05; **, P<0.01).