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Effect of plasma, steroids, or steroid products on the adhesion of human opsonized thrombocytes to human leukocytes.

An in vitro system was designed in which human thrombocytes were opsonized with rabbit antihuman platelet antibody and incubated with human leukocytes in EDTA-plasma in order to measure opsonized platelet-leukocyte adhesion. Antiplatelet antibody opsonization enhanced platelet-leukocyte adhesion 2.6-fold over control nonopsonized platelets in 50 out of 56 experiments. A plasma factor was found necessary for the support of opsonized platelet-leukocyte adhesion. This factor was EDTA-stable, heat labile, and labile to freezing and thawing. Hydrocortisone at 10-2 M was extremely effective in preventing opsonized platelet-leukocyte adhesion in 11 out of 14 experiments (2 S.D. below test-control value). Plasmas from 23 different patients ingesting 20 to 120 mg. of prednisone per day, were also tested. Seventeen out of 23 (74 per cent) did not support opsonized platelet-leukocyte adhesion at in vivo steroid concentrations of 10-6 M. Dilutions of 6 of these plasma samples with pooled normal plasma from 8- to 16-fold were still incapable of supporting opsonized platelet-leukocyte adhesion, whereas higher dilutions were capable. "Nonsteroid" plasma from 9 out of 17 (53 per cent) hospitalized "sick" patients were also incapable of supporting opsonized platelet-leukocyte adhesion. "Steroid plasma" from 5 out of 6 patients with severe thrombocytopenic purpura refractory to steroid treatment, did support leukocyte adhesion of opsonized platelets. It is concluded that a plasma factor is required for opsonized platelet-leukocyte adhesion. A steroid metabolite or byproduct factor is capable of inhibiting the adhesion of antibody-coated human platelets to leukocytes at an in vivo "steroid" concentration of 10-7 M. This factor does not appear to be present in most patients refractory to steroid treatment for autoimmune thrombocytopenic purpura.