Immune impairment of XXXX phagocytosis during influenza virus pneumonia.

@entity5131 @entity19 @entity794 @entity133 @entity358 @entity8667
The pathogenesis of @entity5131 is associated with an intact antiviral immune response. To determine the degree of involvement of the host response in influenza virus-induced @entity358 , @entity19 were immunosuppressed by treatment with @entity8667 ( @entity8667 ). Eight days after infection, pulmonary defense mechanisms were quantitated by aerogenic challenge with @entity794 ; the ingestion of opsonized erythrocyte (EA) was used to monitor the phagocytic capability of alveolar macrophages obtained by pulmonary lavage. The @entity8667 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 @entity8667 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 @entity8667 ameliorated the impairment in phagocytic ingestion, the index being 505 +/- 34. Incubation of alveolar macrophages from virus-infected, @entity8667 -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 @entity133 phagocytosis is, in part, immunologically mediated.
