Passive Deformability of Mature, Immature, and Active Neutrophils in Healthy and Septicemic Neonates

Obstruction of narrow vessels by rigid neutrophils may contribute to ischemic organ injury. In septicemia, a substantial portion of the neutrophils may become activated and the number of circulating immature neutrophils may rise sharply. Volume and deformability of mature (PMN) and immature neutrophils in healthy preterm and full-term infants and in septicemic neonates were studied by means of a micropipette system. Membrane cytoplasm tongues were aspirated into 2.5-µm (diameter) pipettes over a period of 60 s. Volume and tongue growth of mature resting PMN were similar in healthy preterm and full-term neonates and adults. Compared with mature PMN (about 360 fl), the volumes of band cells (415 fl), metamyelocytes (470 fl), and less mature cells (myeloblasts, promyelocytes, and myelocytes; 490 fl) were significantly increased (p < 0.005). Final tongue lengths of band cells, metamyelocytes, and less mature cells were decreased by about 50, 60, and 70%, respectively, when compared with passive mature cells. In septic neonates, the percentage of immature neutrophils was increased, but the deformability and volume of the cell subpopulations were not affected by septicemia. Active PMN were characterized by pseudopod formation. More active PMN were found in group B streptococcal (14% of total PMN), Gram-negative (12%), and Staphylococcus epidermidis septicemia (8%) than in healthy neonates and adults (4%). The main bodies of active PMN were less deformable than passive PMN, and the pseudopods showed very little membrane deformation. The increased number of rigid active and immature neutrophils may contribute to impaired microcirculation and the high risk for organ injury in septic patients.

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