The pathogenesis of viral pneumonia is associated with an intact antiviral immune response. To determine the degree of involvement of the host response in influenza virus-induced impairment of pulmonary antibacterial defenses, mice were immunosuppressed by treatment with antilymphocyte serum (ALS). Eight days after infection, pulmonary defense mechanisms were quantitated by aerogenic challenge with Staphylococcus aureus; the ingestion of opsonized erythrocytes (EA) was used to monitor the phagocytic capability of alveolar macrophages obtained by pulmonary lavage. The ALS treatment alone caused no significant alteration in pulmonary antibacterial defenses or macrophage phagocytosis, nor did it interfere with viral multiplication. In noninfected lungs, less than 1% of the initial viable staphylococci remained viable at 24 h compared with proliferation to 490 ± 147% in virus-infected lungs. Treatment with ALS prevented staphylococcal multiplication, the bactericidal value being 28 ± 12% at the same time period. The phagocytic index (EA ingested/100 macrophages) in cells retrieved from normal lungs was 783 ± 22 compared with 235 ± 29 in macrophages from virus-infected lungs. The ALS ameliorated the impairment in phagocytic ingestion, the index being 505 ± 34. Incubation of alveolar macrophages from virus-infected, ALS-treated animals with specific viral antibody reestablished the phagocytic defect in a dose-dependent manner, the index being 215 ± 30 at the lowest dilution of antiviral globulin. The data demonstrate that the virus-induced suppression of pulmonary antibacterial defenses caused by dysfunction in alveolar macrophage phagocytosis is, in part, immunologically mediated.