Role of peroxiredoxin of the AhpC/TSA family in antioxidant defense mechanisms of Francisella tularensis
Fig 5
The ΔahpC mutant of F. tularensis LVS does not exhibit intramacrophage growth defect, but is attenuated for virulence in mice.
(A) Raw264.7 macrophages were infected with the F. tularensis (Ft) LVS, the ΔahpC mutant or the transcomplemented strain (ΔahpC+pahpC) at 10 and 100 MOI (n = 3 biological replicates). The cells were lysed after 4 and 24 hrs of infection, serially diluted and plated on MH-chocolate agar plates for enumeration of bacterial CFU. The data are representative of three independent experiments conducted and are expressed as Log10 CFU/mL. (B) C57BL/6 and phox-/- mice (n = 4 mice/group) were infected intranasally with 1x104 CFUs of F. tularensis LVS or the ΔahpC mutant and observed for mortality for a period of 21 days post-infection. The results are expressed as Kaplan-Meier survival curves, and the p values were determined using the Log-rank test. The comparison shown is between the wild type mice infected with Ft LVS and the ΔahpC mutant.