Deformability of human granulocytes: Role of calcium and relationship to locomotion

Abstract

We have demonstrated a requirement for Ca 2+ in the induction of deformability changes in the membranes of human polymorphonuclear leukocytes (PMNs). PMN deformability was studied by the technique of cell elastimetry which measures the amount of negative pressure required to aspirate a cell into a small pored micropipet. PMNs incubated in the presence of 5 m M Ca 2+ and the ionophore A23187 (10 −5 M) rapidly became more rigid, i.e., decreased deformability, over a 10- to 15-min period. The effect was noted regardless of order of addition of Ca 2+ or ionophore, but both were required to exert the change. Other divalent cations such as Mg 2+, Mn 2+, or Co 2+ had no effect. When cells rendered rigid by Ca 2+ and ionophore were allowed to stand in suspension, deformability gradually and spontaneously increased, eventually reaching baseline levels. Decreased deformability was again induced by the addition of fresh Ca 2+ and ionophore. Upon standing, cells again increased deformability to baseline, although the time required was significantly longer than following the first addition. Introduction of a competitive inhibitor of transmembrane calcium transport, lanthanum (La 3+) blocked both effects. PMNs treated with both La 3+ and Ca 2− showed no changes in deformability, and introduction of La 3+ to PMN suspensions which had been rendered rigid by Ca 2+ completely blocked the recovery phase. These data establish an active role for Ca 2+ in altering deformability of the PMN and strongly supports our previous hypothesis that chemotactic factors exert their influence upon PMN movement by triggering a sequence which involves Ca 2+-dependent changes in deformability. Abnormalities in this sequence may underlie some of the disorders of human PMN movement.