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First published online April 24, 2006
doi: 10.1242/10.1242/jcs.02876

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Mechanics of neutrophil phagocytosis: experiments and quantitative models

¹ Biomedical Engineering Department, Boston University, 44 Cummington Street, Boston, MA 02215, USA
² Department of Biomedical Engineering, University of California, 451 East Health Sciences Drive, Davis, CA 95616, USA

^* Author for correspondence (e-mail: herantm{at}bu.edu)

Accepted 5 January 2006

To quantitatively characterize the mechanical processes that drive phagocytosis, we observed the FcR-driven engulfment of antibody-coated beads of diameters 3 µm to 11 µm by initially spherical neutrophils. In particular, the time course of cell morphology, of bead motion and of cortical tension were determined. Here, we introduce a number of mechanistic models for phagocytosis and test their validity by comparing the experimental data with finite element computations for multiple bead sizes. We find that the optimal models involve two key mechanical interactions: a repulsion or pressure between cytoskeleton and free membrane that drives protrusion, and an attraction between cytoskeleton and membrane newly adherent to the bead that flattens the cell into a thin lamella. Other models such as cytoskeletal expansion or swelling appear to be ruled out as main drivers of phagocytosis because of the characteristics of bead motion during engulfment. We finally show that the protrusive force necessary for the engulfment of large beads points towards storage of strain energy in the cytoskeleton over a large distance from the leading edge (0.5 µm), and that the flattening force can plausibly be generated by the known concentrations of unconventional myosins at the leading edge.

Key words: Membrane tension, Lamella, Cell mechanics, Cell motility, Finite element simulations

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