Neutrophils from human infants exhibit decreased viability.

The viability of neutrophils, isolated from infant blood and placed into lipid culture, was decreased when compared to that of neutrophils obtained from mothers and controls that had been stored under identical conditions (percentage viable after 20 hr of culture was 49, 75 and 78 for infant, maternal, and control neutrophils, respectively). Increased quantities of hydrogen peroxide were released into the extracellular culture media by nonphagocytic neutrophils from infants (0.25 nM/min/2.5 x 10(6) neutrophils compared to 0.14 for controls), a condition that could promote autooxidation because infant neutrophils are deficient in glutathione peroxidase and catalase (enzymes that detoxify hydrogen peroxide). Results of two studies supported the idea that cell death in culture was related to oxidative damage: (1) phagocytosis induced a loss of viability in maternal and control neutrophils of a similar degree (48 and 52% viable, respectively) to that exhibited by nonphagocytic infant cells (47% viable), a finding prevented by superoxide dismutase and catalase; (2) glucose oxidase-glucose, a hydrogen peroxide-generating system, accelerated death of nonphagocytic neutrophils in culture. It is possible that decreased viability of infant neutrophils is similarly present in vivo (e.g., in inflammatory exudates) and that this finding contributes to the impairment of host defenses.