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. 2016 Feb 24;84(3):735–746. doi: 10.1128/IAI.00942-15

FIG 9.

FIG 9

Deletion of pe19 partially suppresses the replication defect of the ΔpstA1 mutant in NOS2−/− mice. NOS2−/− (A), Irgm1−/− (B), or C57BL/6J (C) mice were infected by the aerosol route with ∼100 CFU of the M. tuberculosis WT, ΔpstA1, ΔpstA1 Δpe19, or Δpe19 strain. Groups of infected mice (n = 4) were euthanized at the indicated time points. Bacterial CFU were enumerated by plating lung homogenates on 7H10 agar and incubating for 3 to 4 weeks at 37°C. Symbols represent means, and error bars indicate standard errors of the means. Results for the ΔpstA1 Δpe19 mutant are from a single experiment and are representative of two independent experiments. All other results are from a single experiment. Asterisks indicate statistically significant differences between ΔpstA1 and ΔpstA1 Δpe19 mutants (*, P < 0.05; **, P < 0.005) (A), between both the ΔpstA1 and ΔpstA1 Δpe19 mutants compared to the WT (*, P < 0.05; **, P < 0.007) (B), and between Δpe19 and WT strains (*, P < 0.05; **, P < 0.005; ***, P < 0.001) (C).