(Click image for movie due to David Rogers, Vanderbilt University. A human neutrophil chases Staphylococcus aureus microorganisms among red blood cells.)

    An even more intriguing situation arises when a cluster of cells execute collective migration, which plays prominent roles in a variety of biological processes ranging from wound healing to neural crest cell migration during embryonic development. How do the cells interact among themselves and coordinate their movement? What signaling proteins and pathways are involved, and how do the chemical signaling interact with mechanotransduction? We have explored these questions in a recent model based on contact inhibition of locomotion and co-attraction.

    We are also interested in the reaction of cells to mechanical forcing and strain. For example, stretch and compression can induce cell fluidization, and neutrophils entering a small microfluidic channel can polarize and activate following fluidization. Accounting for the inhibition of Rac activation by cortical tension, we have modeled Rac growth and potential polarization by a wave-pinning mechanism after the cytoskeleton is fluidized by mechanical strain (full text). The movie below shows a typical simulation of the fluidization of a neutrophil upon entering a narrow channel, and its subsequent activation after exiting.


    (A neutrophil traversing a microfluidic channel with a contraction. The color indicates the magnitude of the membrane modulus as the cell fluidizes and later activates.)

    (A typical simulation of the stretching of a red blood cell by an optical tweezer. The color indicates the magnitude of instantaneous velocity.)

Department of ChBE / Department of Mathematics / Fluids Lab / James J. Feng / Research