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Entry of the bacterial pathogen Listeria monocytogenes into mammalian cells Ireton KCell Microbiol 2007[Jun]; 9 (6): 1365-75The 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.|Animals[MESH]|Bacterial Proteins/metabolism[MESH]|Cadherins/metabolism[MESH]|Humans[MESH]|Listeria monocytogenes/metabolism/*pathogenicity[MESH]|Listeriosis/*microbiology[MESH]|Membrane Proteins/metabolism[MESH]|Receptor Protein-Tyrosine Kinases/metabolism[MESH]|Receptors, Growth Factor/metabolism[MESH]|Signal Transduction[MESH] |
