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Imaging InlC Secretion to Investigate Cellular Infection by the Bacterial Pathogen Listeria monocytogenes
Published on: September 19, 2013
Subversion of cellular functions by Listeria monocytogenes
Javier Pizarro-Cerdá1, Pascale Cossart
1Unité des Interactions Bactéries-Cellules/INSERM U604/INRA USC2020, Institut Pasteur, Paris, France. pizarroj@pasteur.fr
The Journal of Pathology
|December 20, 2005
Summary
Listeria monocytogenes invades host cells using specific proteins like InlA and InlB. It then employs listeriolysin O (LLO) and ActA to escape the vacuole, move in the cytoplasm, and spread between cells.
Area of Science:
- Microbiology
- Cell Biology
- Infectious Diseases
Background:
- Listeria monocytogenes is a significant intracellular pathogen.
- Understanding its invasion and intracellular mechanisms is crucial for combating infections.
Purpose of the Study:
- To elucidate the roles of key virulence factors in the intracellular life cycle of Listeria monocytogenes.
- To detail the molecular mechanisms of bacterial entry, vacuole escape, cytoplasmic movement, and cell-to-cell spread.
Main Methods:
- The study focuses on the functions of specific bacterial proteins: InlA, InlB, Listeriolysin O (LLO), and ActA.
- It examines how these proteins interact with host cell machinery, including E-cadherin, Met receptor, and the actin cytoskeleton.
Main Results:
- InlA facilitates entry into polarized epithelial cells via E-cadherin.
- InlB promotes internalization in non-polarized cells by interacting with the Met receptor.
- LLO lyses the phagocytic vacuole, with its activity regulated by host cell pH.
- ActA drives actin polymerization for bacterial motility and cell-to-cell spread.
Conclusions:
- Listeria monocytogenes employs a sophisticated arsenal of virulence factors to navigate and exploit the host cell environment.
- Targeting these specific bacterial mechanisms offers potential strategies for therapeutic intervention against listeriosis.
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