Complement - Dependent Platelet Injury

Blood platelets are involved in a number of immune reactions and, by release of vasoactive amines and thromboplastic factor(s), may contribute to vascular injury and deposition of fibrin (1, 2). Platelet injury can be induced by bacterial endotoxins (3, 4) and immune complexes (5-7), both of which require complement, and by membrane-active bacterial toxins such as streptolysins O and S and staphylococcal alpha toxin, which act directly on the platelet membrane without the participation of complement (8). Staphylococcal protein A (SPA)] a component of the cell wall of coagulasepositive staphylococci, is known to elicit a number of immune reactions such as Arthus-like reaction in rabbits and immediate skin hypersensitivity in humans (9, 10). SPA is unique among microbial products in that it inteiacts with the Fc portion of immunoglobulin G (IgG) rather than with the antigen-binding site on the Fab portion of the immunoglobulin molecule (11, 12), and fixes complement presumably as a result of this interaction (13). Since some of the immune reactions elicited by SPA, such as the Arthus reaction in rabbits, are thought to involve leukocytes and platelets (14), it seemed pertinent to investigate the interaction of SPA and rabbit platelets in vitro. The results of these studies indicate that (a) SPA does induce rabbit platelet injury, (b) that the reaction requires complement, and (c) that a sharp concentration optimum exists, larger amounts of SPA being inhibitory. Further, evidence was obtained that SPA-induced platelet injury could be separated into two steps; first, "sensitization," an interaction of SPA with a noncomplement plasma factor and platelets, and second, amine "release" due to complement-dependent platelet injury.