Abstract
Polymorphonuclear leucocytes (PMNs) of the newborn show poor movement in vitro toward a chemotactic stimulus, such as zymosan-activated human serum (ZAS). This may result from a defect either in spontaneous movement or in the response of the cells to the stimulus. To identify the defect we studied chemotaxis, chemokinesis and spontaneous movement of cord blood PMNs by agarose assay and by the leading front modification of the Boyden chamber technique. Under agarose, cord PMNs showed much spontaneous movement. This, associated with poor stimulated movement, indicated a defect in the responsiveness of cord PMNs to ZAS. In the membrane filter, cord PMNs migrated spontaneously, and in the presence of ZAS, significantly less than adult cells. The weak spontaneous movement most probably resulted from poor deformability of cord PMNs and contributed to the weak stimulated movement of these cells in the filter. Our results indicate that the impaired chemotaxis was due to a defect in both responsiveness and deformability of cord PMNs rather than to a defect in their intrinsic ability to move.
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