(A and B) CNV or ABX mice were inoculated with LCMV (T1b) or PBS i.v. and (A) splenocytes at 6 hr p.i. or (B) PECs at 12 hr p.i. were immediately fixed to preserve the in vivo STAT1 phosphorylation status of macrophages.
(C) CNV or ABX mice were infected with influenza virus (PR8-GP33). At d3 p.i., alveolar macrophages were sorted from the BAL and in vivo induction of antiviral defense genes was assessed by RT-PCR. Gene expression displayed as fold induction over naive alveolar macrophages from CNV mice. Data representative of two independent experiments with n = 3–5 mice per group.
(D–F) CNV or ABX mice were infected with influenza virus (PR8-GP33). Mice received 30 µg of poly I:C (ABX+pIC group) or PBS (CNV & ABX group) i.n. at d −1 and 100 µg of poly I:C or PBS i.p. at d3. Weight loss (D) and blood oxygen (E) saturation after infection (representative exp. n = 4–6: † signifies mice below 70% initial weight were sacrificed). Weight loss statistics determined by two-way ANOVA.
(F) Survival curve after influenza virus infection. Survival curve is a combination of two independent experiments. CNV n = 10, ABX n = 8, ABX+pIC n = 12. Survival statistics determined by log rank test. *p < 0.05, **p < 0.01, and ***p < 0.001. Data shown are mean ± SEM.