Enzymes altering the binding capacity of human blood eosinophils for IgG antibody-coated erythrocytes (EA).

Blood eosinophils from some patients with an eosinophilia have a higher capacity to bind to IgC antibody-coated red cells (EA) than blood eosinophils from normal people. Twenty per cent of eosinophils from normal blood bound EA, whereas eight of nine patients with hypereosinophilic syndromes and all nine patients with filariasis who were studied had blood eosinophils with EA rosette-forming capacities of between 42 and 89%. High EA binding capacity was reduced in culture, and prednisolone and cytochalasins A and B inhibited normal blood eosinophil EA binding. Normal blood eosinophils developed small increases in EA binding capacity in culture, but marked increases occurred after stimulation with soluble immune complexes, endotoxins and lipid A. Supernatants from granulocytes cultured with zymosan-C3b caused rapid increases in eosinophils EA binding capacity which also occurred with neuraminidase, pronase and trypsin. In vitro alterations in EA rosetting did not require protein synthesis and did not affect eosinophil phagocytic capacity for EA. Substances in culture which did not affect eosinophil EA rosetting capacity included sera from patients with eosinophils with high EA binding capacity and chemotactic substances. Cultured eosinophils also developed an increased capacity to form rosettes with EAC3b, and soluble immune complexes stimulated this further. Conversely, blood eosinophils formed less C3b rosettes when separated from heparinized blood in which C3 activation had occurred. CytochalasinA (but not B) irreversibly inhibited eosinophils EAC3b rosette formation. Trypsin also inhibited, but this effect was reversed within 30 min after washing. It was concluded that eosinophils from normal blood have an intrinsically lwo capacity to bind EA, but that in vivo and in response to stimulation in vitro their ability to bind complexed IgG can approach that seen with blood neutrophils. It is suggested that enzymes in granulocyte secretion products may cause the membrane changes which lead to high eosinophils EA binding capacity. This increase, which can occur separately from alterations in EAC binding or phagocytic capacity, may enable eosinophils to take part more effectively in inflammatory reactions in tissues.