The cell biology of Listeria monocytogenes infection: the intersection of bacterial pathogenesis and cell-mediated immunity.
Listeria monocytogenes has emerged as a remarkably tractable pathogen to dissect basic aspects of cell biology, intracellular pathogenesis, and innate and acquired immunity. In order to maintain its intracellular lifestyle, L. monocytogenes has evolved a number of mechanisms to exploit host processes to grow and spread cell to cell without damaging the host cell. The pore-forming protein listeriolysin O mediates escape from host vacuoles and utilizes multiple fail-safe mechanisms to avoid causing toxicity to infected cells. Once in the cytosol, the L. monocytogenes ActA protein recruits host cell Arp2/3 complexes and enabled/vasodilator-stimulated phosphoprotein family members to mediate efficient actin-based motility, thereby propelling the bacteria into neighboring cells. Alteration in any of these processes dramatically reduces the ability of the bacteria to establish a productive infection in vivo.
Portnoy
Daniel A
DA
Department of Molecular and Cell Biology, University of California, Berkeley 94720, USA. portnoy@uclink4.berkeley.edu
Auerbuch
Victoria
V
Glomski
Ian J
IJ
D000199:Actins / Q000276:immunology / Q000378:metabolism / Q000648:ultrastructure; D000818:Animals; D001427:Bacterial Toxins; D002465:Cell Movement / Q000276:immunology; D005057:Eukaryotic Cells / Q000378:metabolism / Q000382:microbiology* / Q000648:ultrastructure; D006360:Heat-Shock Proteins / Q000276:immunology / Q000378:metabolism; D006460:Hemolysin Proteins; D006790:Host-Parasite Interactions / Q000502:physiology; D006801:Humans; D007111:Immunity, Cellular / Q000502:physiology*; D008089:Listeria monocytogenes / Q000378:metabolism* / Q000472:pathogenicity* / Q000648:ultrastructure; D008088:Listeriosis / Q000378:metabolism* / Q000503:physiopathology; D008954:Models, Biological
D000199:Actins; D001427:Bacterial Toxins; D006360:Heat-Shock Proteins; D006460:Hemolysin Proteins; C038705:hlyA protein, Listeria monocytogenes