(A) Female BALB/c mice were intravenously infected with 107 CFUs of E. coli expressing CNF1, E. coli UTI89ΔhlyA (E. coli
CNF1+), or with the isogenic mutant UTI89ΔhlyA/Δcnf1 (E. coli
CNF1-) or the parental strain UTI89 (E. coli
UTI89) prior to the collection of peripheral blood at 3, 6, 24 and 48 h for the measurement of bacteremia (n = 25–30). The red line indicates the mean values. (B) Female BALB/c mice were intravenously infected with 107 CFUs of the E. coli
CNF1- strain transformed with a control empty plasmid (E. coli
CNF1- pempty), with a plasmid encoding the CNF1-inactive mutant C866S (E. coli
CNF1- pcnf1 C866S) or with a plasmid encoding E. coli CNF1 WT (E. coli
CNF1-pcnf1 WT) prior to the collection of peripheral blood at 3, 6, 24 and 48 h for the measurement of bacteremia (n = 6–12). For both (A) and (B), the data are expressed as the mean ± SEM (n = 6–30) at a *p<0.05. (C) BALB/c mouse survival was monitored for 52 h after intravenous injection of 2.108 CFUs of E. coli
CNF1+ or the isogenic mutant, E. coli
CNF1- (n = 20). *p<0.05 using the Gehan-Breslow-Wilcoxon chi-squared test.