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Physical confinement and phagocytic uptake induce directional migration.
Summer G Paulson1,2, Sophia Liu1,2, Jeremy D Rotty1
1Uniformed Services University of the Health Sciences, Department of Biochemistry, Bethesda, MD, USA, 20814.
Biorxiv : the Preprint Server for Biology
|October 1, 2025
Summary
Physical confinement significantly enhances phagocytosis in microglia by activating the Arp2/3 complex and myosin II. This confinement-induced effect also primes cells for migration, improving immune surveillance.
Area of Science:
- Cell biology
- Immunology
- Biophysics
Background:
- Phagocytosis is a critical immune process typically studied in unconfined conditions.
- The influence of physical confinement on phagocytosis and cell behavior is largely unexplored.
Purpose of the Study:
- To investigate the impact of physical confinement on IgG-mediated phagocytosis in BV-2 microglia-like cells.
- To elucidate the roles of Arp2/3 complex, myosin II, and integrin-dependent adhesion in confinement-modulated phagocytosis and cell priming.
- To explore the phenomenon of 'phagocytic priming' and its dependence on physical state and cytoskeletal elements.
Main Methods:
- Utilized BV-2 microglia-like cells in both confined and unconfined in vitro settings.
- Assayed IgG-mediated phagocytosis and bead uptake.
- Investigated the effects of myosin II disruption, cytochalasin D treatment, and integrin-dependent adhesion.
- Monitored persistent cell migration following phagocytosis to assess phagocytic priming.
Main Results:
- Confinement significantly increased the fraction of phagocytic cells compared to unconfined conditions.
- Arp2/3 complex and myosin II were key contributors to confinement-enhanced phagocytosis.
- Confinement partially rescued phagocytic uptake after myosin II disruption and conferred partial resistance to cytochalasin D.
- Bead uptake induced persistent migration ('phagocytic priming'), requiring integrin-dependent adhesion but not for uptake itself.
- Cytoskeletal requirements for phagocytic priming differed between confined (Myosin II, Arp2/3) and unconfined settings.
Conclusions:
- Physical confinement acts as a potent driver of phagocytosis and influences cytoskeletal dynamics.
- Confinement modulates phagocytic priming, a novel behavior potentially enhancing immune cell surveillance.
- Understanding these confinement effects is crucial for interpreting phagocytosis assays and for comprehending innate immune responses in complex microenvironments.
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