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Modulation of host cell function by Legionella pneumophila type IV effectors
1Section of Microbial Pathogenesis, School of Medicine, Yale University, New Haven, Connecticut 06536, USA. andree.hubber@yale.edu
Annual Review of Cell and Developmental Biology
|October 9, 2010
Summary
Legionella pneumophila bacteria survive inside host cells by injecting proteins that block phagosome-lysosome fusion. This allows the bacteria to replicate within a specialized vacuole, evading immune defenses.
Area of Science:
- Microbiology
- Cell Biology
- Immunology
Background:
- Phagocytic cells like macrophages engulf and destroy microbes via phagosome-lysosome fusion.
- Bacterial pathogens have developed mechanisms to evade this host defense pathway.
- Intracellular survival is crucial for pathogens like Legionella pneumophila.
Purpose of the Study:
- To review the intracellular trafficking mechanisms of Legionella pneumophila.
- To elucidate how bacterial effector proteins manipulate host cell processes.
- To understand the formation of the replicative vacuole by L. pneumophila.
Main Methods:
- Focus on the Dot/Icm secretion system of L. pneumophila.
- Analysis of bacterial protein delivery into the host cell cytosol.
- Investigation of host factor manipulation related to membrane trafficking.
Main Results:
- L. pneumophila utilizes the Dot/Icm system to translocate effector proteins into host cells.
- These proteins target conserved host factors involved in membrane transport.
- This manipulation leads to the formation of a unique endoplasmic reticulum-like vacuole.
Conclusions:
- Legionella pneumophila actively remodels host cell pathways for its survival.
- The Dot/Icm system is central to L. pneumophila's virulence strategy.
- Understanding this process offers insights into host-pathogen interactions and membrane trafficking.
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