Figure 4. IL-18 is essential for IFN-γ production and protection against type A F. tularensis.

(A–C) WT and IL-18^−/− mice were infected with 75 CFU of F. tularensis SchuS4 s.c. Weight loss was recorded (A), and, on day 4 after infection, bacterial burden (B) and splenic IFN-γ production (C) were assayed (n = 5–6 per group). Data are representative of 2 independent experiments. Error bars: body weights and IFN-γ, sem; CFU, sd. *P < 0.05 vs. WT mice as determined via t test. (D) IL-18^−/− mice were infected with 75 CFU of F. tularensis SchuS4 s.c and treated daily with 10⁵ U of IFN-γ or with PBS i.p. On day 4 after infection, the bacterial burden was assayed. Error bars, sd (n = 5 per group). *P < 0.05 vs. PBS-treated mice as determined via t test. (E and F) Serum IL-18 levels were measured in naïve WT animals and also in WT, MyD88^−/−, conditional MyD88-deficient, and Caspase-11^−/− mice 4 d after infection with 75 CFU of F. tularensis SchuS4 s.c. Error bar, sd (n = 4–5/group). No significant differences were detected among infected groups via ANOVA.