Figure 3.
HO-1 in macrophages is required for the generation of immune responses to bacterial and viral infections. (A) Control and HO-1M-KO mice were infected intravenously with 105 CFU L. monocytogenes or with a combination of 105 CFU L. monocytogenes and 200 µg polyI:C, and viability was assayed daily for 14 d. Data are representative of two independent experiments (means ± SEM of nine mice per group). (B) Liver sections from control and HO-1M-KO mice infected intravenously with 105 CFU L. monocytogenes either in the absence (a and b) or presence (c and d) of 100 µg polyI:C were stained with H&E to assess inflammation. Representative sections from two independent experiments with five mice per group are shown. Bars, 100 µM. (C) TEPMs from control (n = 3) and HO-1M-KO (n = 3) mice were infected with L. monocytogenes at different MOIs (circles) or L. monocytogenes and polyI:C (triangles) as indicated, and cell survival was measured by crystal violet staining after 24 h. Data are representative of two independent experiments (means ± SEM of three mice per group). (D) IFN-β production was measured in supernatants from cultures in C (means ± SEM of three mice per group). (E) Control and HO-1M-KO mice were infected with 105 CFU L. monocytogenes or with a combination of 105 CFU L. monocytogenes and 200 µg polyI:C, and IFN-β was measured in sera collected 24 h later. Data are representative of two independent experiments (means ± SEM of six mice per group). (F) TEPMs from control (n = 3) and HO-1M-KO (n = 3) mice were infected with SeV, and IFN-β production was measured in supernatants after 24 h. Data are means ± SD of two independent experiments. (G) TEPMs from control (n = 3) and HO-1M-KO (n = 3) mice were infected with SeV for the indicated time points, and WCEs were probed for p-IRF3 and IRF3 as a loading control. Representative data from two independent experiments are shown. n.d., none detected.