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Published 5 August 2002. doi:10.1083/jcb.200205009
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*Listeria Infections
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© The Rockefeller University Press, 0021-9525/2002/8/409 $5.00
The Journal of Cell Biology, Volume 158, Number 3, August 5, 2002 409-414

Mini-Reviews

 The cell biology of Listeria monocytogenes infection : the intersection of bacterial pathogenesis and cell-mediated immunity



Daniel A. Portnoy1,2, Victoria Auerbuch1 and Ian J. Glomski1

1 Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720
2 The School of Public Health, University of California, Berkeley, CA 94720

Address correspondence to Daniel A. Portnoy, Dept. of Molecular and Cell Biology, 401 Barker Hall, University of California, Berkeley, CA 94703-3200. Tel.: (510) 643-3925. Fax: (510) 643-6791. E-mail: portnoy{at}uclink4.berkeley.edu


Abstract
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.

Key Words: hemolysins; phagosome; virulence; macrophage; actins


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