(131e) Clever Bugs: Microbial Hijacking of the Host Cell Adhesion and Motility Systems

From the research of Stuart Cooper's group and others on biomaterial-centered infections, it is now well known that some pathogenic bacteria cleverly exploit the host's extracellular matrix adhesion molecules to bind to and populate biomaterial surfaces, thereby creating a biofilm relatively protected from host-cell defenses. In a similarly clever manner, some bacteria and viruses, including Listeria, Shigella, Rickettsia, and Vaccinia, exploit host-cell systems to bind and gain entry into host cells, and to transport themselves from cell to cell while remaining hidden from host immune defenses. These microbes first attach to cell surfaces by binding host-cell adhesion receptors (such as integrins or cadherins) to stimulate their engulfment by phagocytosis. Then, following escape from the phagosome, the microbes hijack the host cell's actin polymerization system to form what resembles a ?rocket tail? of polymerizing actin, which is used propel the microbes through the cytoplasm and across membranes to infect neighboring cells. This fascinating process has captured much recent scientific and engineering interest, not only for the insight it provides to normal adhesion and motility mechanisms, but also for the novel ways it suggests for transporting gene- or drug-bearing particles and vesicles into, within, and between cells. This presentation will highlight how engineering analysis of reactions, transport, and mechanics involved in actin-propelled intracellular microbial transport has helped elucidate the fundamental mechanisms underlying this phenomenon, as well as lead to better understanding of the molecular and physical mechanisms of intracellular actin polymerization and actin-based cell motility.