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Phagocytosis is the process by which immune cells engulf and degrade pathogens such as fungi or bacteria. In the Heinrich Lab, we examine phagocytosis by neutrophils, the most abundant white blood cells in humans and the first responders to infection. We use both experiments and computational models to understand the mechanisms behind neutrophil phagocytosis. In my PhD work, I have examined both mechanics and calcium signaling during neutrophil phagocytosis, which I will present as two separate stories in this talk. First, I will summarize our use of one- and two-phase fluid models to examine the dynamics of cell spreading during phagocytosis. By relating computational models to experimental data, we showed that phagocytic spreading requires active force input from the cell and cannot realistically be a passive process solely driven by cell-substrate adhesion. In the second portion, I will present my recent work modeling global changes in calcium concentration during neutrophil phagocytosis. Using a relatively small system of ODEs, we can reproduce key features of our experimental measurements of cytosolic calcium concentration over time. By integrating both mechanics and calcium signaling in future models, we hope to answer key questions about the coupling between intracellular signaling and force production by cells during phagocytosis.

Can also join remotely. Contact organizer for Zoom link.