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Immune-enhanced phagocytic dysfunction in pulmonary macrophages infected with parainfluenza 1 (Sendai) virus
Abstract:
Cultured alveolar macrophages infected with parainfluenza 1 (Sendai) virus were treated with specific antiviral immune serum and their phagocytic activity for opsonized erythrocytes (EA), Candida krusei, and Staphylococcus epidermidis quantitated. Membrane Fc receptor and candida binding activity were unaffected by the viral infection. In contrast, the virus infection decreased the phagocytic ingestion of EA. The addition of immune serum induced new phagocytic defects in that the treatment of virus-infected macrophages decreased the binding of EA and candida and reduced the ingestion of the yeast and the staphylococci. In addition, treatment with immune serum also enhanced the phagocytic defects induced by the virus infection alone, further reducing the binding and ingestion of EA. Neither virus infection nor treatment with immune serum affected the intracellular killing of S. epidermidis. These data demonstrated that virus infection of alveolar macrophages in vitro induce phagocytic defects that are accentuated by the treatment of the macrophages with antiviral antibody.
Insights
Viral infection impairs macrophage phagocytosis. Antiviral immune serum exacerbates these defects, reducing the uptake of pathogens and opsonized erythrocytes. Intracellular killing remains unaffected.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Alveolar macrophages are crucial for lung immunity.
- Viral infections can compromise immune cell function.
- Understanding macrophage phagocytosis is key to immune response.
Purpose of the Study:
- To investigate the impact of parainfluenza virus 1 infection on macrophage phagocytic activity.
- To determine how antiviral immune serum affects phagocytosis in infected macrophages.
- To elucidate the combined effects of viral infection and antibody treatment on macrophage function.
Main Methods:
- Cultured alveolar macrophages were infected with parainfluenza 1 (Sendai) virus.
- Phagocytic activity for opsonized erythrocytes, Candida krusei, and Staphylococcus epidermidis was quantified.
- Cells were treated with specific antiviral immune serum.
Main Results:
- Viral infection reduced the phagocytic ingestion of opsonized erythrocytes.
- Immune serum treatment of infected macrophages impaired binding and ingestion of Candida and Staphylococcus.
- Antiviral serum amplified virus-induced defects in opsonized erythrocyte uptake.
Conclusions:
- In vitro viral infection induces phagocytic defects in alveolar macrophages.
- Antiviral antibody treatment accentuates these defects.
- Macrophage phagocytosis is significantly impaired by combined viral infection and immune serum treatment.