Recognition of Staphylococcus aureus by human phagocytes. Signals and disguises of the bacterial surface

Phagocytic cells provide the host its major defense against invasive Staphylococcus aureus, and the staphylococcal surface, by its influence on phagocyte recognition, is a primary determinant of the function of these cells. The peptidoglycan component of the cell wall plays a key role in both opsonic and chemotactic recognition, mediated by IgG, C3b, and C5a, respectively. While cell wall protein A inhibits opsonic recognition by polymorphonuclear leukocytes, it promotes an opsonin-independent mechanism of phagocytosis by human macrophages which possess cytophilic IgG. By masking cell wall-associated opsonic molecules, capsular polysaccharides inhibit recognition, a phenomenon that is overcome by specific anti-capsular antibodies. It is proposed that impaired phagocyte recognition is a basic element in the pathogenesis of staphylococcal endocarditis, and progress in the prevention and treatment of this infection may depend on understanding the basis for this host defense defect.