Abstract
Although a number of investigators have reported that neonatal PMNs have a profound defect in chemotaxis, almost nothing is known about the pathogenesis of this disorder. In the present study we have examined membrane depolarization and calcium requirements for chemotaxis in neonatal and adult PMNs. Suspension of adult PMNs in calcium deprived media resulted in a decreased chemotactic response to FMLP (19% inhibition; p<0.05). Incubation of adult PMNs with the calcium channel blocking agent verapamil also significantly impaired chemotaxis (32% inhibition p<0.001). In marked contrast, the neonatal PMN demonstrated an enhanced chemotactic response when suspended in calcium deprived media (26% increase; p<0.05) and after incubation with verapamil (57% increase; p<0.001), suggesting that inhibitory levels of intracellular calcium might already exist. Adult and cord blood PMN membrane potential changes in response to FMLP were also studied using the membrane potential-sensitive dye, 3-3' dipenty-loxacarbocyanine and a spectrofluorescence assay. Adult PMNs showed a marked increase in fluorescence emission in response to FMLP (32% increase; p<0.001) indicating significant depolarization of the cell membrane. In contrast, FMLP stimulation of neonatal PMNS failed to evoke any significant change in fluorescence and, thus, membrane potential changes. These data suggest that altered intracellular calcium metabolism may exist in the neonatal PMN, preventing normal membrane depolarization from occurring.
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