Title

Entry of the bacterial pathogen Listeria monocytogenes into mammalian cells

Authors

Authors

K. Ireton

Comments

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Abbreviated Journal Title

Cell Microbiol.

Keywords

HEPATOCYTE GROWTH-FACTOR; GRAM-POSITIVE BACTERIA; CENTRAL-NERVOUS-SYSTEM; INVASION PROTEIN-INLB; E-CADHERIN; ADHERENS; JUNCTIONS; PHOSPHOINOSITIDE 3-KINASE; LIVER-REGENERATION; SIGNALING; PATHWAY; EPITHELIAL-CELLS; Cell Biology; Microbiology

Abstract

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.

Journal Title

Cellular Microbiology

Volume

9

Issue/Number

6

Publication Date

1-1-2007

Document Type

Review

Language

English

First Page

1365

Last Page

1375

WOS Identifier

WOS:000246577400001

ISSN

1462-5814

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