Immune-enhanced phagocytic dysfunction in pulmonary macrophages infected with parainfluenza 1 (Sendai) virus.
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.
D000818:Animals; D002175:Candida / Q000276:immunology; D002478:Cells, Cultured; D004912:Erythrocytes / Q000276:immunology; D007106:Immune Sera / Q000494:pharmacology; D008168:Lung / Q000166:cytology; D008264:Macrophages / Q000187:drug effects / Q000276:immunology*; D051379:Mice; D010222:Parainfluenza Virus 1, Human / Q000276:immunology*; D010585:Phagocyte Bactericidal Dysfunction / Q000276:immunology*; D051381:Rats; D011919:Rats, Inbred Strains; D011961:Receptors, Fc / Q000276:immunology; D013210:Staphylococcus / Q000276:immunology
D007106:Immune Sera; D011961:Receptors, Fc