Activation of neutrophil phagocytosis of complement coated and IgG coated sheep erythrocytes by platelet release products

Abstract

Phagocytosis by human neutrophils of opsonized sheep erythrocytes with rabbit immunoglobulin M and human complement (IgM-EAC^h) and those with rabbit immunoglobulin G (IgG-EA) increased 2-3 times of control neutrophils after treatment with released products from activated platelets (PRPr). The factors in PRPr which augmented IgM-EAC^h phagocytosis were suggested to be adenosine diphosphate (ADP) and triphosphate (ATP) by experiments using apyrase treated PRPr and by direct exposures of neutrophils with these nucleotides. The presence of two other stimulators for phagocytosis of IgG-EA were suggested. One was a macromolecular substance of molecular weight greater than 100 000 and the other was a substance of molecular weight less than 500. The latter may be a prostaglandin because the activity was easily removed by acid-extraction with ethylacetate from the water phase, and because prior incubation of platelets with 10 μg per ml indomethacin deprived PRPr of its low molecular weight activity. Exposure of neutrophils to thromboxane B₂, prostaglandin F₂α and prostaglandin E₂ at the concentration of 10⁻⁶–10⁻⁷ mg/ml actually increased the phagocytosis of IgG-EA. The activity in the macromolecular fraction was not affected by prior incubation of platelets with indomethacin.