Lipopolysaccharide releases a priming substance from platelets that augments the oxidative response of polymorphonuclear neutrophils to chemotactic peptide.

Human neutrophils produce small amounts of O2- when stimulated with the chemotactic peptide F-Met-Leu-Phe; preincubating neutrophils with low concentrations of lipopolysaccharide (LPS) markedly increases this response, an effect referred to as priming. Neutrophil suspensions without mononuclear cells and platelets were insusceptible to priming by 10 ng of LPS; susceptibility was restored by reintroducing platelets, approximately five platelets per neutrophil. Incubation of platelets with 10 ng of LPS/mL released a soluble factor that produced graded priming responses of at least fivefold in neutrophils. The priming factor had the properties of a labile protein and did not resemble previously described mediators derived from platelets. Anthrax toxin, which inhibits priming of neutrophils by LPS, inhibited priming by the platelet factor but not release of the factor from platelets. Thus, the platelet factor mediates a portion of the overall priming effect of LPS and thereby modulates the level of O2- generation by neutrophils.