Alteration of the Cell Periphery During Granulocyte Maturation: Relationship to Cell Function

Physiologic characteristics of the surface of human granulocytes may be important determinants of functional capacity. Studies of immature granulocytes and polymorphonuclear neutrophils (PMN’s) from marrow and blood indicated that immature granulocytes are characterized by a high, neuraminidase-susceptible, negative surface charge density; a high degree of cellular rigidity, as measured by an elastimeter with a micropipette orifice size that approximated estimates of average bone marrow basement membrane pore size (3.5µ); low adhesiveness to glass and plastic; low propensity to aggregate; a slow rate of cell spreading, pseudopod extension, and motility; and a very low rate of phagocytosis. At the myelocyte stage, adhesiveness and phagocytosis, although not prominent, became evident. In contrast PMN’s had a lower negative surface charge density, a higher degree of surface deformability (the entire PMN readily deforming to enter a 3.5µ micropipette whereas the immature granulocyte would not so deform), higher adhesiveness (plastic > glass), a higher propensity to aggregate, a higher rate of cell spreading, pseudopod formation and motility, and a higher rate of phagocytosis. The increased deformability and adhesiveness of the PMN as compared to the immature granulocyte may be a reflection of an altered relationship between relaxing and contracting systems at the cell periphery during maturation and/or changes in the sol-gel state of macromolecules at the cell periphery. This concept is supported by the change in surface properties of the PMN toward those of the immature granulocyte at cold temperature (4°C). The increased deformability and reduced surface negative charge of the PMN could facilitate adhesiveness and pseudopod formation and, thereby, increase cell-surface and cell-particle contact with enhancement of motility and phagocytosis. Hence the exit of PMN from bone marrow and circulation and the functional capacity of the PMN may be determined by a process of cytoplasmic maturation during granulopoiesis that adapts the PMN for its essential cell-extracell interactions.