Deciphering the interplay between the genotoxic and probiotic activities of Escherichia coli Nissle 1917
Fig 6
A clbP deletion, but not a genomic point mutation that inactivates ClbP catalytic domain, impairs EcN protection against the enteric pathogen Salmonella Typhimurium in mice.
C57BL/6 female mice were treated with 20 mg streptomycin per os, then 24 h later infected orally with 109 S. Typhimurium (STm) in PBS or co-administered with 109 S. Typhimurium and 109 EcN wild-type, ΔclbP or clbPS95R strains. (A) The mice were monitored for clinical signs (weight loss, diarrhea, signs of abdominal pain) daily during 4 days. Each point corresponds to the mean clinical score +/- SEM of 10 to 15 animals per group in three independent experiment. The animals were scored blindly (without knowledge of the infecting bacteria) in two of the three experiments. Two-way ANOVA with Bonferroni post-test compared to STm + EcN, a: p<0.05, c: p<0.001. (B) The fecal shedding of STm was examined by enumeration of the feces collected at day 2 and 4 after infection. The median and individual results are shown. One way ANOVA of log-transformed CFU counts compared to STm + PBS, a: p<0.05. (C) Fecal counts of STm and EcN were used to determine the competitive index (CFU STm / CFU EcN). One way ANOVA compared to STm + EcN clbPS95R, a: p<0.05.