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.
|Original language||English (US)|
|Number of pages||10|
|Journal||Scandinavian Journal of Infectious Diseases|
|Issue number||SUPPL. 41|
|State||Published - Jan 1 1983|