  Blood leukocytes can exhibit extensive morphological changes during their
passage through small capillary vessels. The human monocytic THP-1 cell line
was used to explore the metabolic dependence of these shape changes. Cells were
aspirated into micropipettes for determination of the rate of protrusion
formation. They were then released and the kinetics of morphological recovery
was studied. Results were consistent with Evans' model (Blood, 64 : 1028, 1984)
of a viscous liquid droplet surrounded by a tensile membrane. The estimated
values of cytoplasmic viscosity and membrane tension were 162 Pa.s and 0.0142
millinewton/m respectively. The influence of metabolic inhibitors on cell
mechanical behaviour was then studied : results strongly suggested that
deformation involved two sequential phases. The cell elongation rate measured
during the first 30 seconds following the onset of aspiration was unaffected by
azide, an inhibitor of energy production, and it was about doubled by
cytochalasin D, a microfilament inhibitor, and colchicine, a microtubule
inhibitor. However, during the following two minutes, deformation was almost
abolished in cells treated with azide and cytochalasin D, whereas the
protrusion of control cells exhibited about threefold length increase. It is
concluded that, although cells seemed to deform as passive objects, active
metabolic processes were required to allow extensive morphological changes
triggered by external forces.
