Immune complexes in the lungs are capable of inducing adverse responses. Herein we have detailed the formation of immune complexes in the lungs of influenza virus-infected mice and examined their effect on alveolar macrophage defenses. On days 3, 7, 10, 15, and 30 after aerosol infection with influenza A/PR8/34 virus, the acellular pulmonary lavage fluid was tested for viral antigen, specific viral antibody, and immune complexes by immunoassays. Whereas peak viral antigen (day 3) diminished to undetectable levels by day 10, specific viral antibody remained at a low concentration until day 10, after which it rapidly increased. Immune complex concentrations increased through day 7, peaked at day 10, and gradually returned to the control level by day 30. These data demonstrate that immune complexes of detectable size are induced by influenza virus infection during the interface between antigen excess and antibody excess conditions. Since alveolar macrophages are the pivotal phagocytic defense cells in the lung, the ability of normal alveolar macrophages to ingest opsonized erythrocytes was quantitated in the presence of immune complexes from lavage fluid. Immune complexes from day 10 virus-infected lungs caused a dose-dependent suppression of antibody-mediated phagocytosis to 30% of control values. In contrast, although these immune complexes also markedly decreased the phagocytosis of antibody-coated yeast cells, they did not significantly impair the antibody-independent ingestion of unopsonized yeast cells by macrophages. The suppressive effects of immune complexes on alveolar macrophages may, in part, explain the phagocytic dysfunction that occurs 7 to 10 days after influenza virus pneumonia.
The effect of specific immunization on the antibacterial defense mechanisms of the murine lung was assessed against Streptococcus pneumoniae, Staphylococcus aureus, Staphylococcus aureus (Smith), Serratia marcescens, Klebsiella pneumoniae, Proteus mirabilis, and Pseudomonas aeruginosa. Immunization by aerosol inhalation significantly enhanced the intrapulmonary killing of Pseudomonas aeruginosa and Proteus mirabilis but not the remaining organisms. With P. mirabilis, systemic immunization induced higher titers of specific serum agglutinins as compared with local respiratory tract immunization; however, local immunization was more effective in enhancing pulmonary bactericidal activity than was parenteral vaccination. Passive immunity against P. mirabilis or aerogenic challenge with preopsonized P. mirabilis significantly enhanced intrapulmonary killing of the homologous organism. With S. aureus, pulmonary bactericidal activity was not accelerated by aerosol challenge with the preopsonized organism, nor was it accelerated in passively immunized mice. These data demonstrate that the immune enhancement of pulmonary bactericidal activity is governed by the bacterium used for challenge and the route of immunization. The results further demonstrate that with P. mirabilis, antibody-mediated mechanisms are involved in the immune enhancement of pulmonary bactericidal activity.
During viral pneumonitis in mice, lung fluid protein and free lysosomal enzyme activity are increased while macrophage lysosomal enzymes are decreased.We thank Alan Green and Mardel Knight for technical assistance.
Pulmonary defense mechanisms were quantitated in mice that were fed a protein-free diet (PFD) for periods of 2 and 3 weeks. Despite the severe weight loss and emaciation induced by the diet, the bactericidal mechanisms in their lungs were preserved against aerogenic challenges with Staphylococcus aureus, Proteus mirabilis, and Listeria monocytogenes. Phagocytic assays of alveolar macrophages that were retrieved by pulmonary lavage from PFD-fed animals showed a decrease in Fc receptor-mediated binding activity but no alteration in the ingestion of sensitized erythrocytes. In contrast, the PFD induced defects in both the attachment phase and the engulfment phase of the phagocytic process when the challenge organism was Candida krusei. The PFD suppressed the pulmonary inflammatory response after mice were infected with influenza virus strain PR8; such mice also failed to eliminate infectious virus from their lungs. Virus infection in control mice suppressed pulmonary antibacterial defenses against challenges with S. aureus and P. mirabilis, a defect that was ameliorated in the lungs of PFD-fed mice with viral pneumonia. The data demonstrated that pulmonary defense mechanisms were modulated by a PFD but that the observed effect was dependent on the agent used to test host defenses.
Intrapulmonary killing of Staphylococcus aureus proceeded at equal rates in guinea pigs, hamsters, rats, and mice. In the lungs of guinea pigs and hamsters, Proteus mirabilis was killed at virtually the same rate as S. aureus as compared with half the rate of inactivation in the lungs of rats and mice.
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