Opsonin-independent phagocytosis of surface-adherent bacteria by human alveolar macrophages.
Opsonin-independent mechanisms of phagocytosis may be important in host defense of certain body sites such as the lung. In this study, one such mechanism, "surface phagocytosis," was investigated by measuring the uptake of unopsonized [3H]-labeled Staphylococcus aureus and Pseudomonas aeruginosa adherent to a plastic surface by human alveolar macrophages (AM) and peripheral blood polymorphonuclear leukocytes (PMN). Efficient uptake of unopsonized bacteria by both cell types was observed. Electron microscopic studies suggested that the manner in which these cell types encounter adherent bacteria is different. While AM appear to gather in organisms at their periphery as they spread out upon the underlying substrate, PMN seem to sweep bacteria up as they move along the plastic surface. Bacterial killing determined by a fluorochrome microassay was decreased by AM compared to PMN. Although the precise mechanism whereby phagocytes recognize unopsonized bacteria adherent to a surface remains to be determined, this aspect of phagocytic cell function may prove to have clinical relevance.
D002462:Cell Membrane / Q000648:ultrastructure; D003550:Cystic Fibrosis / Q000276:immunology; D006801:Humans; D008264:Macrophages / Q000276:immunology* / Q000648:ultrastructure; D008855:Microscopy, Electron, Scanning; D009504:Neutrophils / Q000276:immunology* / Q000648:ultrastructure; D009895:Opsonin Proteins; D010587:Phagocytosis; D011550:Pseudomonas aeruginosa / Q000276:immunology; D013211:Staphylococcus aureus / Q000276:immunology
D009895:Opsonin Proteins