Phagocytosis and destruction of Staphylococcus aureus.
A review is presented for the phagocytosis and intracellular killing of Staphylococcus aureus by polymorphonuclear and mononuclear leukocytes. Recruitment of adequate numbers of leukocytes to the site of infection occurs through the process of chemotaxis. Recognition of invading staphylococci by the phagocytic cells is mediated through bacterial opsonization. Both processes depend upon the activation of the heat-labile complement system which generates the majority of chemotactic (C5a) and opsonic (C3b) molecules for S. aureus phagocytosis. The key role of peptidoglycan in the cell wall of staphylococci in these events is stressed. Attachment and ingestion of opsonized staphylococci occurs via poorly-defined receptors for opsonins in the membrane of the leukocyte. The greater phagocytic capacity of neutrophils as compared to monocytes is not reflected in differences in their membrane receptors for staphylococcal opsonins. Once ingested, staphylococci are rapidly destroyed by oxygen-dependent and oxygen-independent bactericidal mechanisms of the phagocytes. Small numbers of S. aureus may survive within the leukocyte. Special attention is focused on the numerous ways S. aureus is able to hinder, evade, and directly damage the phagocytic defense mechanisms of the host.
D002462:Cell Membrane; D002470:Cell Survival; D002634:Chemotaxis, Leukocyte; D003167:Complement Activation; D009000:Monocytes / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D009895:Opsonin Proteins; D010587:Phagocytosis; D011971:Receptors, Immunologic; D013211:Staphylococcus aureus / Q000276:immunology*
D009895:Opsonin Proteins; D011971:Receptors, Immunologic