First published online April 24, 2006
doi: 10.1242/10.1242/jcs.02876
Journal of Cell Science 119, 1903-1913 (2006)
Published by The Company of Biologists 2006
Mechanics of neutrophil phagocytosis: experiments and quantitative models
Marc Herant1,*,
Volkmar Heinrich2 and
Micah Dembo1
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

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Fig. 1. (A) The pedestal-phase, during which the cell body acquires a slight indentation. (B) The cup-phase, during which lamellae sharply emerge from the cell body to spread over the bead. Notice the distinctive contact angle between cell body and lamella (inset). (C) The rounding-phase, during which the cell rounds up, the contact angle between cell body and lamella vanishes and the bead is pulled inwards.
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Fig. 2. Schematic description of a mechanical model of neutrophil phagocytosis. The cell-bead interface is stabilized by adhesion sites that act as anchors to the internal cytoskeleton. Myosin motors draw down F-actin, thus pulling the bead into the cell or, equivalently, the cell onto the bead. Polymerization of new actin near the contact line (the leading edge) drives protrusion around the bead.
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Fig. 4. Same as previous figure for the phagocytosis of 6.2 µm (top) and 11.2 µm (bottom) beads.
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Fig. 5. Structure of the lamella for the 4.6 µm phagocytosis at 55 seconds (see boxed area in Fig. 3). (Top) Cytoskeletal volume fraction and velocity field with respect to the bead (substratum frame). (Bottom) Polymerization messenger concentration and cytoskeletal velocity field with respect to the cell (lamella frame). The white patch of membrane corresponds to the region of enhanced messenger emissivity. Notice that, the velocity of the cytoskeleton vanishes in the substratum frame at the cell-bead interface due to the no-slip boundary condition. Notice also the high density of cytoskeleton at that same interface due to the contractile force directed down toward the substratum.
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Fig. 6. Comparison of simulations with and without contractile flattening force; 3.2 µm bead (left), 6.2 µm bead (right); with contractility (top), without contractility (bottom).
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Fig. 7. Bead position vs time for simulations of the phagocytosis of a 3.2 µm bead. Solid lines correspond to cytoskeleton-membrane repulsion models, dashed lines to cytoskeletal swelling models. For each model, the flattening force was varied by ±33% around the best fit (thick line). Notice the strong dependence of the bead-trajectory in the cytoskeleton swelling model. Notice also that, for the best fit in this model, the shape of the cell at 20 seconds shows a phagocytic cup of excessive thickness compared with observations.
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© The Company of Biologists Ltd 2006