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Updated: Jul 15, 2026
Imaging InlC Secretion to Investigate Cellular Infection by the Bacterial Pathogen Listeria monocytogenes
Published on: September 19, 2013
Entry of the bacterial pathogen Listeria monocytogenes into mammalian cells
1Department of Molecular Biology and Microbiology, Burnett College of Biomedical Sciences, University of Central Florida, Orlando, Fl 32826-3227, USA. kireton@mail.ucf.edu
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.
Insights
Listeria monocytogenes uses two distinct entry pathways into host cells, mediated by InlA and InlB surface proteins binding to E-cadherin and Met receptors, respectively. Understanding these bacterial entry mechanisms is key to combating foodborne illness.
Area of Science:
- Microbiology
- Cell Biology
- Infectious Diseases
Background:
- Listeria monocytogenes is a foodborne pathogen causing severe illnesses like meningitis and abortion.
- Bacterial entry into non-phagocytic host cells (e.g., epithelial cells, hepatocytes) is crucial for Listeria's virulence and dissemination.
- Two primary bacterial surface proteins, InlA and InlB, mediate Listeria's internalization via distinct host receptor interactions.
Purpose of the Study:
- To elucidate the distinct molecular mechanisms of Listeria monocytogenes internalization into host cells.
- To compare and contrast the signaling pathways and host factors involved in InlA- and InlB-mediated bacterial entry.
- To explore the roles of E-cadherin and Met receptors in Listeria pathogenesis and normal cellular functions.
Main Methods:
- Review and discussion of existing literature on Listeria internalization pathways.
- Analysis of host signaling cascades, cytoskeletal rearrangements, and protein interactions.
- Comparison of adherens junction components (InlA) versus Met-associated signaling (InlB).
Main Results:
- InlA-mediated entry utilizes adherens junction components linked to F-actin and myosin.
- InlB-dependent entry involves Met receptor signaling, phosphoinositide 3-kinase, and Arp2/3 complex activators.
- InlB-mediated entry unexpectedly incorporates endocytic pathway components.
- Distinct host signaling proteins are employed in the two Listeria entry routes.
Conclusions:
- Listeria monocytogenes employs sophisticated and divergent strategies for host cell invasion.
- Understanding the specific molecular players in InlA and InlB pathways offers targets for therapeutic intervention.
- Further research into these pathways may reveal novel insights into the physiological roles of E-cadherin and Met.
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