Entry of the bacterial pathogen Listeria monocytogenes into mammalian cells

Summary The bacterial pathogen Listeria monocytogenes causes food‐borne illnesses leading to meningitis or abortion. Listeria provokes its internalization (‘entry’) into mammalian cells that are normally non‐phagocytic, such as intestinal epithelial cells and hepatocytes. Entry provides access to a nutrient‐rich cytosol and allows translocation across anatomical barriers. Here I discuss the two major internalization pathways used by Listeria . These pathways are initiated by binding of the bacterial surface proteins InlA or InlB to their respective host receptors, E‐cadherin or Met. InlA mediates traversal of the intestinal barrier, whereas InlB promotes infection of the liver. At the cellular level, both InlA‐ and InlB‐dependent entry require host signalling that promotes cytoskeletal rearrangements and pathogen engulfment. However, many of the specific signalling proteins in the two entry routes differ. InlA‐mediated uptake uses components of adherens junctions that are coupled to F‐actin and myosin, whereas InlB‐dependent entry involves cytosolic adaptors that bridge Met to regulators of F‐actin, including phosphoinositide 3‐kinase and activators of the Arp2/3 complex. Unexpectedly, entry directed by InlB also involves endocytic components. Future work on InlA and InlB will lead to a better understanding of virulence, and may also provide novel insights into the normal biological functions of E‐cadherin and Met.