879 ABNORMAL CONCANAVALIN A CAPPING – ANOTHER DEFECT OF NEUTROPHILS FROM HUMAN INFANTS

Abstract

Concanavalin A (con A) binds to neutrophil (N) plasma membranes and induces granule exocytosis, chemotaxis and increased oxidative metabolism. Con A binds diffusely to the N surface, but caps form on N exposed to colchicine or to oxidants (a process dependent on interactions of plasma membrane, cytoskeleton and several biochemical systems). To test the competency of these interactions, we studied fluorescein con A capping of N isolated from venous blood of newborns, their mothers and adult controls. Diffuse con A binding occurred readily, but capping of infant and maternal N was decreased (p < .05). Colchicine induced capping in 38 ± 3, 51 ± 3 and 69 ± 2 (mean % ± SEM) of N from 20 infants, mothers and controls. The oxidant, diamide, induced caps in 45 ± 8, 59 ± 11 and 82 ± 6% respectively. The decreased response was striking because spontaneous capping (without induction) was higher in infants (23% ± 3) and mothers (38% ± 4) than in controls (14% ± 3). Thus, the mean increment in capped N induced by colchicine was 15, 13 and 55% respectively. Spontaneous capping seemed related to oxidation since values were reduced ≅ 70% (p < .05) when N were exposed to superoxide dismutase and catalase. Thus, spontaneous and induced con A capping of infant and maternal N are abnormal, perhaps due to autooxidation. Many cellular processes are involved, and study of this abnormality may identify mechanisms responsible for the other dysfunctions of infant N.