Summaryalso show defective chemotaxis, thereby suggesting an association --between capping and movement in PMNS.-P~Y~~~P~~~~~~~~~ leukocytes (PMNs) have previPMNs from normal human neonates also show deficient themously been shown be chemotactically deficient' To probe the otaxis (2,4,8). To better characterize the nature of this defect, we mechanism(s) responsible for this deficiency, we have investigated studied capping in neonatal PMNs, both spontaneously and in the phenomenon of concanavalin A-induced capping in neonatal response to with colchicine. PMNs. PMNs horn cord blood of 17 healthy, full-term infants and 17 normal adult volunteers were isolated by standard Ficoll-Hypaque and dextran sedimentation. After incubation with and without colchicine, the cells were reincubated with fluorescein isothiocyanate-Con A, fixed, and prepared in wet mounts. Using a fluorescence microscope, PMNs were identified, and the percentage of the capped cells was counted.Upon treatment with colchicine, adult PMNs showed a significant increase in the percentage of capped cells. By contrast, the cord blood PMNs showed no significant increase in capping after colchicine treatment. The difference between percentage of PMNs showing colchicine-induced capping in adult and cord blood was highly significant ( P < 0.01; Student's t test). SpeculationIncreasing evidence suggests that a primary developmental deficiency of neonatal polymorphonuclear leukocyte movement plays an important role in the compromised inflammatory response characteristic of this period of life. The data presented in this report strengthen the argument that the level a t which the developmental deficiency operates is at the cell membrane. Future studies should be directed towards determining whether this represents a primary membrane abnormality or, rather, reflects a defect of cytoskeletal or other submembranous components. Such knowledge-would hopefully lead to improved therapeutic enhancement of the efficiency of neonatal polymorphonuclear leukocyte movement.Chemotaxis of human polymorphonuclear leukocytes (PMNs) involves interactions between the cell membrane and several cytoplasmic cytoskeletal elements-the microtubules and microfilaments. The precise nature of these relationships, however, is unclear. Among the available in vitro probes for characterizing these interactions is "capping," or the accumulation of ligandreceptor complexes at a localized site (9).In lymphocytes, capping can be induced by incubation with polyvalent ligands such as antibodies.Capping in normal human PMNs can abo be demonstrated after exposure to the lectin, concanavalin A (Con A). In normal PMNs, however, Con A capping is significantly increased by incubation of cells with an agent such as colchine, a microtubule disrupter (6).By contrast, PMNs from patients with Chediak-Higashi syndrome do not require preincubation with colchicine and will significantly cap just upon Con A treatment (6, 7). Such PMNs MATERIALS AND METHODSCord blood from normal human term neonates was obtained imm...

Cross-sectional and limited sequential studies of neutrophil and monocyte chemotaxis were done using cells isolated from cord blood and peripheral blood of 2- to 6-day-old neonates and infants at 4 and 6 months of age. These studies show that cord blood phagocyte chemotaxis is comparable to adult values, whereas phagocyte chemotaxis at 2-6 days of age is significantly lower than adult (P less than 0.01) or cord (P less 0.01) chemotaxis values. At 6 months of age, phagocyte chemotaxis is still low compared to adult values (P less than 0.01).

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