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© The Rockefeller University Press, 0021-9525/1999/9/1333/ $5.00
The Journal of Cell Biology, Volume 146, Number 6, September 20, 1999 1333-1350

Listeria monocytogenes Exploits Normal Host Cell Processes to Spread from Cell to Cell

Jennifer R. Robbinsa, Angela I. Barthb, Hélène Marquisc, Eugenio L. de Hostosd, W. James Nelsonb, and Julie A. Theriota,e
a Department of Biochemistry, Stanford University School of Medicine
b Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, California 94305-5307
c Department of Microbiology, University of Colorado Health Sciences Center, Denver, Colorado 80262
d Tropical Disease Research Unit, University of California, San Francisco, California 94121
e Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305-5307

Correspondence to: Julie A. Theriot, Department of Biochemistry, Beckman Center, Stanford School of Medicine, Stanford, CA 94305-5307. Tel:(650) 725-7968 Fax:(650) 723-6783 E-mail:theriot{at}cmgm.stanford.edu.

The bacterial pathogen, Listeria monocytogenes, grows in the cytoplasm of host cells and spreads intercellularly using a form of actin-based motility mediated by the bacterial protein ActA. Tightly adherent monolayers of MDCK cells that constitutively express GFP-actin were infected with L. monocytogenes, and intercellular spread of bacteria was observed by video microscopy. The probability of formation of membrane-bound protrusions containing bacteria decreased with host cell monolayer age and the establishment of extensive cell-cell contacts. After their extension into a recipient cell, intercellular membrane-bound protrusions underwent a period of bacterium-dependent fitful movement, followed by their collapse into a vacuole and rapid vacuolar lysis. Actin filaments in protrusions exhibited decreased turnover rates compared with bacterially associated cytoplasmic actin comet tails. Recovery of motility in the recipient cell required 1–2 bacterial generations. This delay may be explained by acid-dependent cleavage of ActA by the bacterial metalloprotease, Mpl. Importantly, we have observed that low levels of endocytosis of neighboring MDCK cell surface fragments occurs in the absence of bacteria, implying that intercellular spread of bacteria may exploit an endogenous process of paracytophagy.

Key Words: Listeria monocytogenes, ActA, actin, epithelial cells, bacterial pathogenesis


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