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Platelet-mediated antibacterial activity against gram-negative microorganisms has been investigated. Data show that human washed platelets possess the ability to partially inhibit growth of Salmonella typhi Ty-2 (a smooth strain) but not of two rough strains of Salmonella minnesota (R345-Rb and R595-Re). On the other hand, no antibacterial activity was noted in the presence of the gram-positive Staphylococcus aureus. This activity is dependent on the length of incubation of platelets with bacteria and apparently is not mediated by platelet soluble factors. Finally, lysis of platelets with Triton X-100 following their incubation with bacteria gives rise to the same degree of antibacterial activity observed in the untreated samples. This implies that the described platelet function does not rely on the possible trapping of bacteria in platelet aggregates.

The in vitro effect of a purified endotoxin preparation from culture fluids of Shigella sonnei, phase I (purified free endotoxin, PFE) and of three endotoxin preparations chemically extracted from the intact parent cells on human blood mononuclear leucocytes and platelets was investigated. PFE, like cell-extracted preparations, caused generation of strong procoagulant activity (tissue factor) by human mononuclear cells. PFE-stimulated cells, however, developed significantly greater activity than cells stimulated by the other endotoxins. they had about 4-fold more activity. Neither free nor cell-extracted preparations induced aggregation in human citrated or heparinized platelet-rich plasma (PRP) or unmasking of platelet factor 3 (PF3). These findings suggest that free endotoxin from Shigella sonnei, phase I resembles endotoxin extracted from cells by conventional procedures in their interaction with human platelets and mononuclear leucocytes. In view of the possible contribution of free endotoxin to endotoxemia in human and experimental gram-negative sepsis, our data that free endotoxin stimulates human mononuclear leucocytes to produce a potent trigger of blood coagulation (tissue factor) may be relevant to the understanding of the mechanism(s) responsible for the initiation of intravascular coagulation in severe human infections.

Some effects of bacterial endotoxin on leukocytes and platelets are reviewed. The release of two mediators, Leukocyte Inhibiting Factor (LIF) and Tissue Factor (TF) from human mononuclear cells are described. These factors may play either beneficial effects (LIF) or noxious activities (TF liberation in certain pathological conditions). Regarding the activities of LPS on platelets the AA. report some personal data about the electrokinetic modification of platelets due to endotoxin. This LPS effect can be performed directly or via a lymphokine release, Platelet Slowing Factor (PSF). In the light of all the mentioned considerations, a scheme of interaction LPS/platelets is suggested.