Opsonin-reversible resistance of Mycoplasma pneumoniae to in vitro phagocytosis by alveolar macrophages.
Several species of mycoplasmas are responsible for respiratory disease in animals and man. As yet, little is known about the interaction of these pathogens with alveolar macrophages, one of the primary components of pulmonary resistance to infections. The present study was undertaken to develop an in vitro model to examine this organism-cell interaction, using a human pathogen, mycoplasma pneumoniae, and normal guinea pig alveolar macrophages. During a 24-h incubation of M. pneumoniae with a monolayer of macrophages, mycoplasmas were found to attach directly to the surface of the cells without inducing significant phagocytosis. Ultrastructurally, the organisms appeared bound to the cell membrane by their characteristic attachment organelles. Only after the addition of specific anti-mycoplasma serum were cells able to engulf attached and surrounding organisms. These data suggest that the interaction of M. pneumoniae and alveolar macrophages is a potentially important aspect of disease pathogenesis, and immune factors which might alter this interaction merit further examination.
D000818:Animals; D001345:Autoradiography; D002448:Cell Adhesion; D006168:Guinea Pigs; D007106:Immune Sera; D007111:Immunity, Cellular; D008264:Macrophages / Q000276:immunology* / Q000648:ultrastructure; D008854:Microscopy, Electron; D008858:Microscopy, Phase-Contrast; D009174:Mycoplasma / Q000276:immunology* / Q000648:ultrastructure; D009895:Opsonin Proteins; D010587:Phagocytosis; D011650:Pulmonary Alveoli / Q000166:cytology; D011817:Rabbits / Q000276:immunology; D013936:Thymidine / Q000378:metabolism; D014316:Tritium
D007106:Immune Sera; D009895:Opsonin Proteins; D014316:Tritium; D013936:Thymidine