Title

Entry Of The Bacterial Pathogen Listeria Monocytogenes Into Mammalian Cells

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. © 2007 The Authors; Journal compilation © 2007 Blackwell Publishing Ltd.

Publication Date

6-1-2007

Publication Title

Cellular Microbiology

Volume

9

Issue

6

Number of Pages

1365-1375

Document Type

Article

Personal Identifier

scopus

DOI Link

https://doi.org/10.1111/j.1462-5822.2007.00933.x

Socpus ID

34248645155 (Scopus)

Source API URL

https://api.elsevier.com/content/abstract/scopus_id/34248645155

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